The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury
Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Abd El-Fattah, Eslam E. [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2022transfer abstract |
|---|
| Schlagwörter: |
|---|
| Übergeordnetes Werk: |
Enthalten in: A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a - Liao, Gary ELSEVIER, 2020, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:147 ; year:2022 ; pages:0 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.biopha.2022.112628 |
|---|
| Katalog-ID: |
ELV056805500 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV056805500 | ||
| 003 | DE-627 | ||
| 005 | 20230626044011.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 220808s2022 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.biopha.2022.112628 |2 doi | |
| 028 | 5 | 2 | |a /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001835.pica |
| 035 | |a (DE-627)ELV056805500 | ||
| 035 | |a (ELSEVIER)S0753-3322(22)00016-6 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | 4 | |a 610 |q VZ |
| 084 | |a 44.86 |2 bkl | ||
| 100 | 1 | |a Abd El-Fattah, Eslam E. |e verfasserin |4 aut | |
| 245 | 1 | 4 | |a The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury |
| 264 | 1 | |c 2022transfer abstract | |
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. | ||
| 520 | |a Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. | ||
| 650 | 7 | |a MCP-1 |2 Elsevier | |
| 650 | 7 | |a SOD |2 Elsevier | |
| 650 | 7 | |a ICAM-1 |2 Elsevier | |
| 650 | 7 | |a MDA |2 Elsevier | |
| 650 | 7 | |a LPS |2 Elsevier | |
| 650 | 7 | |a SGLT-2 |2 Elsevier | |
| 650 | 7 | |a ASC |2 Elsevier | |
| 650 | 7 | |a NF-κB |2 Elsevier | |
| 650 | 7 | |a TNF-α |2 Elsevier | |
| 650 | 7 | |a CAT |2 Elsevier | |
| 650 | 7 | |a ROS |2 Elsevier | |
| 650 | 7 | |a AMPK |2 Elsevier | |
| 650 | 7 | |a NLRP3 |2 Elsevier | |
| 650 | 7 | |a TGF-β |2 Elsevier | |
| 650 | 7 | |a GSH |2 Elsevier | |
| 650 | 7 | |a TLR4 |2 Elsevier | |
| 650 | 7 | |a ALI |2 Elsevier | |
| 650 | 7 | |a IPF |2 Elsevier | |
| 700 | 1 | |a Saber, Sameh |4 oth | |
| 700 | 1 | |a Mourad, Ahmed A.E. |4 oth | |
| 700 | 1 | |a El-Ahwany, Eman |4 oth | |
| 700 | 1 | |a Amin, Noha A. |4 oth | |
| 700 | 1 | |a Cavalu, Simona |4 oth | |
| 700 | 1 | |a Yahya, Galal |4 oth | |
| 700 | 1 | |a Saad, Ahmed S. |4 oth | |
| 700 | 1 | |a Alsharidah, Mansour |4 oth | |
| 700 | 1 | |a Shata, Ahmed |4 oth | |
| 700 | 1 | |a Sami, Haidy M. |4 oth | |
| 700 | 1 | |a Kaddah, Mohamed M.Y. |4 oth | |
| 700 | 1 | |a Ghanim, Amal M.H. |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Liao, Gary ELSEVIER |t A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a |d 2020 |g Amsterdam [u.a.] |w (DE-627)ELV004620771 |
| 773 | 1 | 8 | |g volume:147 |g year:2022 |g pages:0 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.biopha.2022.112628 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 912 | |a SSG-OLC-PHA | ||
| 936 | b | k | |a 44.86 |j Hämatologie |q VZ |
| 951 | |a AR | ||
| 952 | |d 147 |j 2022 |h 0 | ||
| author_variant |
e f e e a efee efeea |
|---|---|
| matchkey_str |
abdelfattaheslamesabersamehmouradahmedae:2022----:hdnmcnepabtenmkfsgaignnr3snwhrpuitreiifamtoeegnrlodpgilznnvr |
| hierarchy_sort_str |
2022transfer abstract |
| bklnumber |
44.86 |
| publishDate |
2022 |
| allfields |
10.1016/j.biopha.2022.112628 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001835.pica (DE-627)ELV056805500 (ELSEVIER)S0753-3322(22)00016-6 DE-627 ger DE-627 rakwb eng 610 VZ 44.86 bkl Abd El-Fattah, Eslam E. verfasserin aut The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. MCP-1 Elsevier SOD Elsevier ICAM-1 Elsevier MDA Elsevier LPS Elsevier SGLT-2 Elsevier ASC Elsevier NF-κB Elsevier TNF-α Elsevier CAT Elsevier ROS Elsevier AMPK Elsevier NLRP3 Elsevier TGF-β Elsevier GSH Elsevier TLR4 Elsevier ALI Elsevier IPF Elsevier Saber, Sameh oth Mourad, Ahmed A.E. oth El-Ahwany, Eman oth Amin, Noha A. oth Cavalu, Simona oth Yahya, Galal oth Saad, Ahmed S. oth Alsharidah, Mansour oth Shata, Ahmed oth Sami, Haidy M. oth Kaddah, Mohamed M.Y. oth Ghanim, Amal M.H. oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:147 year:2022 pages:0 https://doi.org/10.1016/j.biopha.2022.112628 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 147 2022 0 |
| spelling |
10.1016/j.biopha.2022.112628 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001835.pica (DE-627)ELV056805500 (ELSEVIER)S0753-3322(22)00016-6 DE-627 ger DE-627 rakwb eng 610 VZ 44.86 bkl Abd El-Fattah, Eslam E. verfasserin aut The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. MCP-1 Elsevier SOD Elsevier ICAM-1 Elsevier MDA Elsevier LPS Elsevier SGLT-2 Elsevier ASC Elsevier NF-κB Elsevier TNF-α Elsevier CAT Elsevier ROS Elsevier AMPK Elsevier NLRP3 Elsevier TGF-β Elsevier GSH Elsevier TLR4 Elsevier ALI Elsevier IPF Elsevier Saber, Sameh oth Mourad, Ahmed A.E. oth El-Ahwany, Eman oth Amin, Noha A. oth Cavalu, Simona oth Yahya, Galal oth Saad, Ahmed S. oth Alsharidah, Mansour oth Shata, Ahmed oth Sami, Haidy M. oth Kaddah, Mohamed M.Y. oth Ghanim, Amal M.H. oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:147 year:2022 pages:0 https://doi.org/10.1016/j.biopha.2022.112628 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 147 2022 0 |
| allfields_unstemmed |
10.1016/j.biopha.2022.112628 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001835.pica (DE-627)ELV056805500 (ELSEVIER)S0753-3322(22)00016-6 DE-627 ger DE-627 rakwb eng 610 VZ 44.86 bkl Abd El-Fattah, Eslam E. verfasserin aut The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. MCP-1 Elsevier SOD Elsevier ICAM-1 Elsevier MDA Elsevier LPS Elsevier SGLT-2 Elsevier ASC Elsevier NF-κB Elsevier TNF-α Elsevier CAT Elsevier ROS Elsevier AMPK Elsevier NLRP3 Elsevier TGF-β Elsevier GSH Elsevier TLR4 Elsevier ALI Elsevier IPF Elsevier Saber, Sameh oth Mourad, Ahmed A.E. oth El-Ahwany, Eman oth Amin, Noha A. oth Cavalu, Simona oth Yahya, Galal oth Saad, Ahmed S. oth Alsharidah, Mansour oth Shata, Ahmed oth Sami, Haidy M. oth Kaddah, Mohamed M.Y. oth Ghanim, Amal M.H. oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:147 year:2022 pages:0 https://doi.org/10.1016/j.biopha.2022.112628 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 147 2022 0 |
| allfieldsGer |
10.1016/j.biopha.2022.112628 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001835.pica (DE-627)ELV056805500 (ELSEVIER)S0753-3322(22)00016-6 DE-627 ger DE-627 rakwb eng 610 VZ 44.86 bkl Abd El-Fattah, Eslam E. verfasserin aut The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. MCP-1 Elsevier SOD Elsevier ICAM-1 Elsevier MDA Elsevier LPS Elsevier SGLT-2 Elsevier ASC Elsevier NF-κB Elsevier TNF-α Elsevier CAT Elsevier ROS Elsevier AMPK Elsevier NLRP3 Elsevier TGF-β Elsevier GSH Elsevier TLR4 Elsevier ALI Elsevier IPF Elsevier Saber, Sameh oth Mourad, Ahmed A.E. oth El-Ahwany, Eman oth Amin, Noha A. oth Cavalu, Simona oth Yahya, Galal oth Saad, Ahmed S. oth Alsharidah, Mansour oth Shata, Ahmed oth Sami, Haidy M. oth Kaddah, Mohamed M.Y. oth Ghanim, Amal M.H. oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:147 year:2022 pages:0 https://doi.org/10.1016/j.biopha.2022.112628 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 147 2022 0 |
| allfieldsSound |
10.1016/j.biopha.2022.112628 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001835.pica (DE-627)ELV056805500 (ELSEVIER)S0753-3322(22)00016-6 DE-627 ger DE-627 rakwb eng 610 VZ 44.86 bkl Abd El-Fattah, Eslam E. verfasserin aut The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. MCP-1 Elsevier SOD Elsevier ICAM-1 Elsevier MDA Elsevier LPS Elsevier SGLT-2 Elsevier ASC Elsevier NF-κB Elsevier TNF-α Elsevier CAT Elsevier ROS Elsevier AMPK Elsevier NLRP3 Elsevier TGF-β Elsevier GSH Elsevier TLR4 Elsevier ALI Elsevier IPF Elsevier Saber, Sameh oth Mourad, Ahmed A.E. oth El-Ahwany, Eman oth Amin, Noha A. oth Cavalu, Simona oth Yahya, Galal oth Saad, Ahmed S. oth Alsharidah, Mansour oth Shata, Ahmed oth Sami, Haidy M. oth Kaddah, Mohamed M.Y. oth Ghanim, Amal M.H. oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:147 year:2022 pages:0 https://doi.org/10.1016/j.biopha.2022.112628 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 147 2022 0 |
| language |
English |
| source |
Enthalten in A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a Amsterdam [u.a.] volume:147 year:2022 pages:0 |
| sourceStr |
Enthalten in A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a Amsterdam [u.a.] volume:147 year:2022 pages:0 |
| format_phy_str_mv |
Article |
| bklname |
Hämatologie |
| institution |
findex.gbv.de |
| topic_facet |
MCP-1 SOD ICAM-1 MDA LPS SGLT-2 ASC NF-κB TNF-α CAT ROS AMPK NLRP3 TGF-β GSH TLR4 ALI IPF |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a |
| authorswithroles_txt_mv |
Abd El-Fattah, Eslam E. @@aut@@ Saber, Sameh @@oth@@ Mourad, Ahmed A.E. @@oth@@ El-Ahwany, Eman @@oth@@ Amin, Noha A. @@oth@@ Cavalu, Simona @@oth@@ Yahya, Galal @@oth@@ Saad, Ahmed S. @@oth@@ Alsharidah, Mansour @@oth@@ Shata, Ahmed @@oth@@ Sami, Haidy M. @@oth@@ Kaddah, Mohamed M.Y. @@oth@@ Ghanim, Amal M.H. @@oth@@ |
| publishDateDaySort_date |
2022-01-01T00:00:00Z |
| hierarchy_top_id |
ELV004620771 |
| dewey-sort |
3610 |
| id |
ELV056805500 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV056805500</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230626044011.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">220808s2022 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.biopha.2022.112628</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">/cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001835.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV056805500</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0753-3322(22)00016-6</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.86</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Abd El-Fattah, Eslam E.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="4"><subfield code="a">The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022transfer abstract</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">MCP-1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">SOD</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">ICAM-1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">MDA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">LPS</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">SGLT-2</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">ASC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NF-κB</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TNF-α</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CAT</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">ROS</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">AMPK</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NLRP3</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TGF-β</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">GSH</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TLR4</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">ALI</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IPF</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Saber, Sameh</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Mourad, Ahmed A.E.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">El-Ahwany, Eman</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Amin, Noha A.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Cavalu, Simona</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yahya, Galal</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Saad, Ahmed S.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Alsharidah, Mansour</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Shata, Ahmed</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sami, Haidy M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kaddah, Mohamed M.Y.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ghanim, Amal M.H.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Liao, Gary ELSEVIER</subfield><subfield code="t">A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a</subfield><subfield code="d">2020</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV004620771</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:147</subfield><subfield code="g">year:2022</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.biopha.2022.112628</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.86</subfield><subfield code="j">Hämatologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">147</subfield><subfield code="j">2022</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| author |
Abd El-Fattah, Eslam E. |
| spellingShingle |
Abd El-Fattah, Eslam E. ddc 610 bkl 44.86 Elsevier MCP-1 Elsevier SOD Elsevier ICAM-1 Elsevier MDA Elsevier LPS Elsevier SGLT-2 Elsevier ASC Elsevier NF-κB Elsevier TNF-α Elsevier CAT Elsevier ROS Elsevier AMPK Elsevier NLRP3 Elsevier TGF-β Elsevier GSH Elsevier TLR4 Elsevier ALI Elsevier IPF The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury |
| authorStr |
Abd El-Fattah, Eslam E. |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV004620771 |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 VZ 44.86 bkl The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury MCP-1 Elsevier SOD Elsevier ICAM-1 Elsevier MDA Elsevier LPS Elsevier SGLT-2 Elsevier ASC Elsevier NF-κB Elsevier TNF-α Elsevier CAT Elsevier ROS Elsevier AMPK Elsevier NLRP3 Elsevier TGF-β Elsevier GSH Elsevier TLR4 Elsevier ALI Elsevier IPF Elsevier |
| topic |
ddc 610 bkl 44.86 Elsevier MCP-1 Elsevier SOD Elsevier ICAM-1 Elsevier MDA Elsevier LPS Elsevier SGLT-2 Elsevier ASC Elsevier NF-κB Elsevier TNF-α Elsevier CAT Elsevier ROS Elsevier AMPK Elsevier NLRP3 Elsevier TGF-β Elsevier GSH Elsevier TLR4 Elsevier ALI Elsevier IPF |
| topic_unstemmed |
ddc 610 bkl 44.86 Elsevier MCP-1 Elsevier SOD Elsevier ICAM-1 Elsevier MDA Elsevier LPS Elsevier SGLT-2 Elsevier ASC Elsevier NF-κB Elsevier TNF-α Elsevier CAT Elsevier ROS Elsevier AMPK Elsevier NLRP3 Elsevier TGF-β Elsevier GSH Elsevier TLR4 Elsevier ALI Elsevier IPF |
| topic_browse |
ddc 610 bkl 44.86 Elsevier MCP-1 Elsevier SOD Elsevier ICAM-1 Elsevier MDA Elsevier LPS Elsevier SGLT-2 Elsevier ASC Elsevier NF-κB Elsevier TNF-α Elsevier CAT Elsevier ROS Elsevier AMPK Elsevier NLRP3 Elsevier TGF-β Elsevier GSH Elsevier TLR4 Elsevier ALI Elsevier IPF |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
s s ss a a m aa aam e e a eea n a a na naa s c sc g y gy a s s as ass m a ma a s as h m s hm hms m m k mm mmk a m g am amg |
| hierarchy_parent_title |
A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a |
| hierarchy_parent_id |
ELV004620771 |
| dewey-tens |
610 - Medicine & health |
| hierarchy_top_title |
A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV004620771 |
| title |
The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury |
| ctrlnum |
(DE-627)ELV056805500 (ELSEVIER)S0753-3322(22)00016-6 |
| title_full |
The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury |
| author_sort |
Abd El-Fattah, Eslam E. |
| journal |
A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a |
| journalStr |
A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology |
| recordtype |
marc |
| publishDateSort |
2022 |
| contenttype_str_mv |
zzz |
| container_start_page |
0 |
| author_browse |
Abd El-Fattah, Eslam E. |
| container_volume |
147 |
| class |
610 VZ 44.86 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Abd El-Fattah, Eslam E. |
| doi_str_mv |
10.1016/j.biopha.2022.112628 |
| dewey-full |
610 |
| title_sort |
dynamic interplay between ampk/nfκb signaling and nlrp3 is a new therapeutic target in inflammation: emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury |
| title_auth |
The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury |
| abstract |
Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. |
| abstractGer |
Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. |
| abstract_unstemmed |
Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA |
| title_short |
The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury |
| url |
https://doi.org/10.1016/j.biopha.2022.112628 |
| remote_bool |
true |
| author2 |
Saber, Sameh Mourad, Ahmed A.E. El-Ahwany, Eman Amin, Noha A. Cavalu, Simona Yahya, Galal Saad, Ahmed S. Alsharidah, Mansour Shata, Ahmed Sami, Haidy M. Kaddah, Mohamed M.Y. Ghanim, Amal M.H. |
| author2Str |
Saber, Sameh Mourad, Ahmed A.E. El-Ahwany, Eman Amin, Noha A. Cavalu, Simona Yahya, Galal Saad, Ahmed S. Alsharidah, Mansour Shata, Ahmed Sami, Haidy M. Kaddah, Mohamed M.Y. Ghanim, Amal M.H. |
| ppnlink |
ELV004620771 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth oth oth oth oth oth oth oth oth |
| doi_str |
10.1016/j.biopha.2022.112628 |
| up_date |
2024-07-06T21:27:11.310Z |
| _version_ |
1803866583924211712 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV056805500</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230626044011.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">220808s2022 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.biopha.2022.112628</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">/cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001835.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV056805500</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0753-3322(22)00016-6</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.86</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Abd El-Fattah, Eslam E.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="4"><subfield code="a">The dynamic interplay between AMPK/NFκB signaling and NLRP3 is a new therapeutic target in inflammation: Emerging role of dapagliflozin in overcoming lipopolysaccharide-mediated lung injury</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022transfer abstract</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Acute lung injury (ALI) is one the most common causes of morbidity and mortality in critically ill patients. In this study, we examined for first time the role of dapagliflozin (DPGZ) in lipopolysaccharide (LPS)-induced ALI in rats and determined the underlying molecular mechanisms by evaluating the effects of DPGZ on adenosine monophosphate kinase (AMPK), nuclear transcription factor kappa B, nucleotide-binding and oligomerization domain-like receptor 3 inflammasome activation. Treatment of acute lung injured rats with either low dose (5 mg/kg) or high dose (10 mg/kg) DPGZ significantly decreased oxidative stress by decreasing malondialdehyde and nitric oxide tissue levels with a significant increase in spectrophotometric measurements of superoxide dismutase, catalase, and reduced glutathione levels. DPGZ treatment resulted in a significant anti-inflammatory effect as indicated by suppression in myeloperoxidase activity, MCP-1, IL-1β, IL-18, and TNF-α levels. DPGZ treatment also increased p-AMPK/t-AMPK with a significant reduction in NF-kB P65 binding activity and NFĸB p65 (pSer536) levels. These effects of DPGZ were accompanied by a significant reduction in NLRP3 levels and NLRP3 gene expression and a significant decrease in caspase-1 activity, which were also confirmed by histopathological examinations. We conclude that DPGZ antioxidant and anti-inflammatory activity may occur through regulation of AMPK/NFĸB pathway and inhibition of NLRP3 activation. These results suggest that DPGZ represents a promising intervention for the treatment of ALI, particularly in patients with type 2 diabetes.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">MCP-1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">SOD</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">ICAM-1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">MDA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">LPS</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">SGLT-2</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">ASC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NF-κB</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TNF-α</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CAT</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">ROS</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">AMPK</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NLRP3</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TGF-β</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">GSH</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TLR4</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">ALI</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IPF</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Saber, Sameh</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Mourad, Ahmed A.E.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">El-Ahwany, Eman</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Amin, Noha A.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Cavalu, Simona</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yahya, Galal</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Saad, Ahmed S.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Alsharidah, Mansour</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Shata, Ahmed</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sami, Haidy M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kaddah, Mohamed M.Y.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ghanim, Amal M.H.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Liao, Gary ELSEVIER</subfield><subfield code="t">A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a</subfield><subfield code="d">2020</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV004620771</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:147</subfield><subfield code="g">year:2022</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.biopha.2022.112628</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.86</subfield><subfield code="j">Hämatologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">147</subfield><subfield code="j">2022</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| score |
7.400193 |