Hesperetin ameliorates spinal cord injury by inhibiting NLRP3 inflammasome activation and pyroptosis through enhancing Nrf2 signaling
Neuroinflammation is a prominent feature of traumatic spinal cord injuries (SCIs). Hesperetin exhibits anti-inflammatory effects in neurological disorders; however, the potential neuroprotective effects of hesperetin in cases of SCI remain unclear. Sprague-Dawley rats with C5 hemi-contusion injuries...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Liu, Zhongyuan [verfasserIn] Tu, Kewu [verfasserIn] Zou, Peiqian [verfasserIn] Liao, Congrui [verfasserIn] Ding, Ruoting [verfasserIn] Huang, Zucheng [verfasserIn] Huang, Zhiping [verfasserIn] Yao, Xinqiang [verfasserIn] Chen, Jianting [verfasserIn] Zhang, Zhongmin [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2023 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: International immunopharmacology - Amsterdam [u.a.] : Elsevier Science, 2001, 118 |
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| Übergeordnetes Werk: |
volume:118 |
| DOI / URN: |
10.1016/j.intimp.2023.110103 |
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| Katalog-ID: |
ELV009560637 |
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| 245 | 1 | 0 | |a Hesperetin ameliorates spinal cord injury by inhibiting NLRP3 inflammasome activation and pyroptosis through enhancing Nrf2 signaling |
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| 520 | |a Neuroinflammation is a prominent feature of traumatic spinal cord injuries (SCIs). Hesperetin exhibits anti-inflammatory effects in neurological disorders; however, the potential neuroprotective effects of hesperetin in cases of SCI remain unclear. Sprague-Dawley rats with C5 hemi-contusion injuries were used as an SCI model. Hesperetin was administered to the experimental rats in order to investigate its neuroprotective effects after SCI, and BV2 cells were pretreated with hesperetin or silencing of nuclear factor erythroid 2-related factor 2 (siNrf2), and then stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). The therapeutic impact and molecular mechanism of hesperetin were elucidated in a series of in vivo and in vitro investigations conducted using a combination of experiments. The results of the present in vivo experiment indicated that hesperetin improved functional recovery and protected spinal cord tissue after SCI. Hesperetin attenuated oxidative stress and microglial activation, lowered malondialdehyde (MDA) levels, and elevated catalase (CAT), glutathione (GSH)-Px, and superoxide dismutase (SOD) levels. Moreover, hesperetin downregulated the expression of advanced oxygenation protein products (AOPPs), ionized calcium-binding adapter molecule 1 (Iba-1), NOD-like receptor protein 3 (NLRP3), and interleukin-1 beta (IL-1β), but increased the expression of Nrf2. In vitro studies have shown that hesperetin inhibits the generation of reactive oxygen species (ROS), as well as the neuroinflammation associated with the upregulation of Nrf2 and heme oxygenase-1 (HO-1) in BV2 cells. The results of the present study indicated that hesperetin inhibited BV2 cell pyroptosis and significantly blocked the expression of NLRP3 inflammasome proteins (NLRP3 Caspase-1 p10 apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain [ASC]) and pro-inflammatory mediators (IL-18, IL-1β). Furthermore, the silencing of Nrf2 by small interfering ribonucleic acid (siRNA) partially abolished its antioxidant effect in the aforementioned cell experiments. Collectively, these findings illustrate that through an increase in Nrf2 signaling hesperetin reduces oxidative stress and neuroinflammation by suppressing NLRP3 inflammasome activation and pyroptosis. | ||
| 650 | 4 | |a Hesperetin | |
| 650 | 4 | |a Neuroinflammation | |
| 650 | 4 | |a Oxidative stress | |
| 650 | 4 | |a Nrf2 signaling pathway | |
| 650 | 4 | |a NLRP3-mediated pyroptosis | |
| 700 | 1 | |a Tu, Kewu |e verfasserin |4 aut | |
| 700 | 1 | |a Zou, Peiqian |e verfasserin |4 aut | |
| 700 | 1 | |a Liao, Congrui |e verfasserin |4 aut | |
| 700 | 1 | |a Ding, Ruoting |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, Zucheng |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, Zhiping |e verfasserin |4 aut | |
| 700 | 1 | |a Yao, Xinqiang |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Jianting |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Zhongmin |e verfasserin |4 aut | |
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10.1016/j.intimp.2023.110103 doi (DE-627)ELV009560637 (ELSEVIER)S1567-5769(23)00424-1 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Liu, Zhongyuan verfasserin (orcid)0000-0002-7794-243X aut Hesperetin ameliorates spinal cord injury by inhibiting NLRP3 inflammasome activation and pyroptosis through enhancing Nrf2 signaling 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Neuroinflammation is a prominent feature of traumatic spinal cord injuries (SCIs). Hesperetin exhibits anti-inflammatory effects in neurological disorders; however, the potential neuroprotective effects of hesperetin in cases of SCI remain unclear. Sprague-Dawley rats with C5 hemi-contusion injuries were used as an SCI model. Hesperetin was administered to the experimental rats in order to investigate its neuroprotective effects after SCI, and BV2 cells were pretreated with hesperetin or silencing of nuclear factor erythroid 2-related factor 2 (siNrf2), and then stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). The therapeutic impact and molecular mechanism of hesperetin were elucidated in a series of in vivo and in vitro investigations conducted using a combination of experiments. The results of the present in vivo experiment indicated that hesperetin improved functional recovery and protected spinal cord tissue after SCI. Hesperetin attenuated oxidative stress and microglial activation, lowered malondialdehyde (MDA) levels, and elevated catalase (CAT), glutathione (GSH)-Px, and superoxide dismutase (SOD) levels. Moreover, hesperetin downregulated the expression of advanced oxygenation protein products (AOPPs), ionized calcium-binding adapter molecule 1 (Iba-1), NOD-like receptor protein 3 (NLRP3), and interleukin-1 beta (IL-1β), but increased the expression of Nrf2. In vitro studies have shown that hesperetin inhibits the generation of reactive oxygen species (ROS), as well as the neuroinflammation associated with the upregulation of Nrf2 and heme oxygenase-1 (HO-1) in BV2 cells. The results of the present study indicated that hesperetin inhibited BV2 cell pyroptosis and significantly blocked the expression of NLRP3 inflammasome proteins (NLRP3 Caspase-1 p10 apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain [ASC]) and pro-inflammatory mediators (IL-18, IL-1β). Furthermore, the silencing of Nrf2 by small interfering ribonucleic acid (siRNA) partially abolished its antioxidant effect in the aforementioned cell experiments. Collectively, these findings illustrate that through an increase in Nrf2 signaling hesperetin reduces oxidative stress and neuroinflammation by suppressing NLRP3 inflammasome activation and pyroptosis. Hesperetin Neuroinflammation Oxidative stress Nrf2 signaling pathway NLRP3-mediated pyroptosis Tu, Kewu verfasserin aut Zou, Peiqian verfasserin aut Liao, Congrui verfasserin aut Ding, Ruoting verfasserin aut Huang, Zucheng verfasserin aut Huang, Zhiping verfasserin aut Yao, Xinqiang verfasserin aut Chen, Jianting verfasserin aut Zhang, Zhongmin verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 118 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:118 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.38 Pharmakologie AR 118 |
| spelling |
10.1016/j.intimp.2023.110103 doi (DE-627)ELV009560637 (ELSEVIER)S1567-5769(23)00424-1 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Liu, Zhongyuan verfasserin (orcid)0000-0002-7794-243X aut Hesperetin ameliorates spinal cord injury by inhibiting NLRP3 inflammasome activation and pyroptosis through enhancing Nrf2 signaling 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Neuroinflammation is a prominent feature of traumatic spinal cord injuries (SCIs). Hesperetin exhibits anti-inflammatory effects in neurological disorders; however, the potential neuroprotective effects of hesperetin in cases of SCI remain unclear. Sprague-Dawley rats with C5 hemi-contusion injuries were used as an SCI model. Hesperetin was administered to the experimental rats in order to investigate its neuroprotective effects after SCI, and BV2 cells were pretreated with hesperetin or silencing of nuclear factor erythroid 2-related factor 2 (siNrf2), and then stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). The therapeutic impact and molecular mechanism of hesperetin were elucidated in a series of in vivo and in vitro investigations conducted using a combination of experiments. The results of the present in vivo experiment indicated that hesperetin improved functional recovery and protected spinal cord tissue after SCI. Hesperetin attenuated oxidative stress and microglial activation, lowered malondialdehyde (MDA) levels, and elevated catalase (CAT), glutathione (GSH)-Px, and superoxide dismutase (SOD) levels. Moreover, hesperetin downregulated the expression of advanced oxygenation protein products (AOPPs), ionized calcium-binding adapter molecule 1 (Iba-1), NOD-like receptor protein 3 (NLRP3), and interleukin-1 beta (IL-1β), but increased the expression of Nrf2. In vitro studies have shown that hesperetin inhibits the generation of reactive oxygen species (ROS), as well as the neuroinflammation associated with the upregulation of Nrf2 and heme oxygenase-1 (HO-1) in BV2 cells. The results of the present study indicated that hesperetin inhibited BV2 cell pyroptosis and significantly blocked the expression of NLRP3 inflammasome proteins (NLRP3 Caspase-1 p10 apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain [ASC]) and pro-inflammatory mediators (IL-18, IL-1β). Furthermore, the silencing of Nrf2 by small interfering ribonucleic acid (siRNA) partially abolished its antioxidant effect in the aforementioned cell experiments. Collectively, these findings illustrate that through an increase in Nrf2 signaling hesperetin reduces oxidative stress and neuroinflammation by suppressing NLRP3 inflammasome activation and pyroptosis. Hesperetin Neuroinflammation Oxidative stress Nrf2 signaling pathway NLRP3-mediated pyroptosis Tu, Kewu verfasserin aut Zou, Peiqian verfasserin aut Liao, Congrui verfasserin aut Ding, Ruoting verfasserin aut Huang, Zucheng verfasserin aut Huang, Zhiping verfasserin aut Yao, Xinqiang verfasserin aut Chen, Jianting verfasserin aut Zhang, Zhongmin verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 118 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:118 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.38 Pharmakologie AR 118 |
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10.1016/j.intimp.2023.110103 doi (DE-627)ELV009560637 (ELSEVIER)S1567-5769(23)00424-1 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Liu, Zhongyuan verfasserin (orcid)0000-0002-7794-243X aut Hesperetin ameliorates spinal cord injury by inhibiting NLRP3 inflammasome activation and pyroptosis through enhancing Nrf2 signaling 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Neuroinflammation is a prominent feature of traumatic spinal cord injuries (SCIs). Hesperetin exhibits anti-inflammatory effects in neurological disorders; however, the potential neuroprotective effects of hesperetin in cases of SCI remain unclear. Sprague-Dawley rats with C5 hemi-contusion injuries were used as an SCI model. Hesperetin was administered to the experimental rats in order to investigate its neuroprotective effects after SCI, and BV2 cells were pretreated with hesperetin or silencing of nuclear factor erythroid 2-related factor 2 (siNrf2), and then stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). The therapeutic impact and molecular mechanism of hesperetin were elucidated in a series of in vivo and in vitro investigations conducted using a combination of experiments. The results of the present in vivo experiment indicated that hesperetin improved functional recovery and protected spinal cord tissue after SCI. Hesperetin attenuated oxidative stress and microglial activation, lowered malondialdehyde (MDA) levels, and elevated catalase (CAT), glutathione (GSH)-Px, and superoxide dismutase (SOD) levels. Moreover, hesperetin downregulated the expression of advanced oxygenation protein products (AOPPs), ionized calcium-binding adapter molecule 1 (Iba-1), NOD-like receptor protein 3 (NLRP3), and interleukin-1 beta (IL-1β), but increased the expression of Nrf2. In vitro studies have shown that hesperetin inhibits the generation of reactive oxygen species (ROS), as well as the neuroinflammation associated with the upregulation of Nrf2 and heme oxygenase-1 (HO-1) in BV2 cells. The results of the present study indicated that hesperetin inhibited BV2 cell pyroptosis and significantly blocked the expression of NLRP3 inflammasome proteins (NLRP3 Caspase-1 p10 apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain [ASC]) and pro-inflammatory mediators (IL-18, IL-1β). Furthermore, the silencing of Nrf2 by small interfering ribonucleic acid (siRNA) partially abolished its antioxidant effect in the aforementioned cell experiments. Collectively, these findings illustrate that through an increase in Nrf2 signaling hesperetin reduces oxidative stress and neuroinflammation by suppressing NLRP3 inflammasome activation and pyroptosis. Hesperetin Neuroinflammation Oxidative stress Nrf2 signaling pathway NLRP3-mediated pyroptosis Tu, Kewu verfasserin aut Zou, Peiqian verfasserin aut Liao, Congrui verfasserin aut Ding, Ruoting verfasserin aut Huang, Zucheng verfasserin aut Huang, Zhiping verfasserin aut Yao, Xinqiang verfasserin aut Chen, Jianting verfasserin aut Zhang, Zhongmin verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 118 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:118 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.38 Pharmakologie AR 118 |
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10.1016/j.intimp.2023.110103 doi (DE-627)ELV009560637 (ELSEVIER)S1567-5769(23)00424-1 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Liu, Zhongyuan verfasserin (orcid)0000-0002-7794-243X aut Hesperetin ameliorates spinal cord injury by inhibiting NLRP3 inflammasome activation and pyroptosis through enhancing Nrf2 signaling 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Neuroinflammation is a prominent feature of traumatic spinal cord injuries (SCIs). Hesperetin exhibits anti-inflammatory effects in neurological disorders; however, the potential neuroprotective effects of hesperetin in cases of SCI remain unclear. Sprague-Dawley rats with C5 hemi-contusion injuries were used as an SCI model. Hesperetin was administered to the experimental rats in order to investigate its neuroprotective effects after SCI, and BV2 cells were pretreated with hesperetin or silencing of nuclear factor erythroid 2-related factor 2 (siNrf2), and then stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). The therapeutic impact and molecular mechanism of hesperetin were elucidated in a series of in vivo and in vitro investigations conducted using a combination of experiments. The results of the present in vivo experiment indicated that hesperetin improved functional recovery and protected spinal cord tissue after SCI. Hesperetin attenuated oxidative stress and microglial activation, lowered malondialdehyde (MDA) levels, and elevated catalase (CAT), glutathione (GSH)-Px, and superoxide dismutase (SOD) levels. Moreover, hesperetin downregulated the expression of advanced oxygenation protein products (AOPPs), ionized calcium-binding adapter molecule 1 (Iba-1), NOD-like receptor protein 3 (NLRP3), and interleukin-1 beta (IL-1β), but increased the expression of Nrf2. In vitro studies have shown that hesperetin inhibits the generation of reactive oxygen species (ROS), as well as the neuroinflammation associated with the upregulation of Nrf2 and heme oxygenase-1 (HO-1) in BV2 cells. The results of the present study indicated that hesperetin inhibited BV2 cell pyroptosis and significantly blocked the expression of NLRP3 inflammasome proteins (NLRP3 Caspase-1 p10 apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain [ASC]) and pro-inflammatory mediators (IL-18, IL-1β). Furthermore, the silencing of Nrf2 by small interfering ribonucleic acid (siRNA) partially abolished its antioxidant effect in the aforementioned cell experiments. Collectively, these findings illustrate that through an increase in Nrf2 signaling hesperetin reduces oxidative stress and neuroinflammation by suppressing NLRP3 inflammasome activation and pyroptosis. Hesperetin Neuroinflammation Oxidative stress Nrf2 signaling pathway NLRP3-mediated pyroptosis Tu, Kewu verfasserin aut Zou, Peiqian verfasserin aut Liao, Congrui verfasserin aut Ding, Ruoting verfasserin aut Huang, Zucheng verfasserin aut Huang, Zhiping verfasserin aut Yao, Xinqiang verfasserin aut Chen, Jianting verfasserin aut Zhang, Zhongmin verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 118 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:118 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.38 Pharmakologie AR 118 |
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10.1016/j.intimp.2023.110103 doi (DE-627)ELV009560637 (ELSEVIER)S1567-5769(23)00424-1 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Liu, Zhongyuan verfasserin (orcid)0000-0002-7794-243X aut Hesperetin ameliorates spinal cord injury by inhibiting NLRP3 inflammasome activation and pyroptosis through enhancing Nrf2 signaling 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Neuroinflammation is a prominent feature of traumatic spinal cord injuries (SCIs). Hesperetin exhibits anti-inflammatory effects in neurological disorders; however, the potential neuroprotective effects of hesperetin in cases of SCI remain unclear. Sprague-Dawley rats with C5 hemi-contusion injuries were used as an SCI model. Hesperetin was administered to the experimental rats in order to investigate its neuroprotective effects after SCI, and BV2 cells were pretreated with hesperetin or silencing of nuclear factor erythroid 2-related factor 2 (siNrf2), and then stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). The therapeutic impact and molecular mechanism of hesperetin were elucidated in a series of in vivo and in vitro investigations conducted using a combination of experiments. The results of the present in vivo experiment indicated that hesperetin improved functional recovery and protected spinal cord tissue after SCI. Hesperetin attenuated oxidative stress and microglial activation, lowered malondialdehyde (MDA) levels, and elevated catalase (CAT), glutathione (GSH)-Px, and superoxide dismutase (SOD) levels. Moreover, hesperetin downregulated the expression of advanced oxygenation protein products (AOPPs), ionized calcium-binding adapter molecule 1 (Iba-1), NOD-like receptor protein 3 (NLRP3), and interleukin-1 beta (IL-1β), but increased the expression of Nrf2. In vitro studies have shown that hesperetin inhibits the generation of reactive oxygen species (ROS), as well as the neuroinflammation associated with the upregulation of Nrf2 and heme oxygenase-1 (HO-1) in BV2 cells. The results of the present study indicated that hesperetin inhibited BV2 cell pyroptosis and significantly blocked the expression of NLRP3 inflammasome proteins (NLRP3 Caspase-1 p10 apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain [ASC]) and pro-inflammatory mediators (IL-18, IL-1β). Furthermore, the silencing of Nrf2 by small interfering ribonucleic acid (siRNA) partially abolished its antioxidant effect in the aforementioned cell experiments. Collectively, these findings illustrate that through an increase in Nrf2 signaling hesperetin reduces oxidative stress and neuroinflammation by suppressing NLRP3 inflammasome activation and pyroptosis. Hesperetin Neuroinflammation Oxidative stress Nrf2 signaling pathway NLRP3-mediated pyroptosis Tu, Kewu verfasserin aut Zou, Peiqian verfasserin aut Liao, Congrui verfasserin aut Ding, Ruoting verfasserin aut Huang, Zucheng verfasserin aut Huang, Zhiping verfasserin aut Yao, Xinqiang verfasserin aut Chen, Jianting verfasserin aut Zhang, Zhongmin verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 118 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:118 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.38 Pharmakologie AR 118 |
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Liu, Zhongyuan @@aut@@ Tu, Kewu @@aut@@ Zou, Peiqian @@aut@@ Liao, Congrui @@aut@@ Ding, Ruoting @@aut@@ Huang, Zucheng @@aut@@ Huang, Zhiping @@aut@@ Yao, Xinqiang @@aut@@ Chen, Jianting @@aut@@ Zhang, Zhongmin @@aut@@ |
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2023-01-01T00:00:00Z |
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Hesperetin exhibits anti-inflammatory effects in neurological disorders; however, the potential neuroprotective effects of hesperetin in cases of SCI remain unclear. Sprague-Dawley rats with C5 hemi-contusion injuries were used as an SCI model. Hesperetin was administered to the experimental rats in order to investigate its neuroprotective effects after SCI, and BV2 cells were pretreated with hesperetin or silencing of nuclear factor erythroid 2-related factor 2 (siNrf2), and then stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). The therapeutic impact and molecular mechanism of hesperetin were elucidated in a series of in vivo and in vitro investigations conducted using a combination of experiments. The results of the present in vivo experiment indicated that hesperetin improved functional recovery and protected spinal cord tissue after SCI. Hesperetin attenuated oxidative stress and microglial activation, lowered malondialdehyde (MDA) levels, and elevated catalase (CAT), glutathione (GSH)-Px, and superoxide dismutase (SOD) levels. Moreover, hesperetin downregulated the expression of advanced oxygenation protein products (AOPPs), ionized calcium-binding adapter molecule 1 (Iba-1), NOD-like receptor protein 3 (NLRP3), and interleukin-1 beta (IL-1β), but increased the expression of Nrf2. In vitro studies have shown that hesperetin inhibits the generation of reactive oxygen species (ROS), as well as the neuroinflammation associated with the upregulation of Nrf2 and heme oxygenase-1 (HO-1) in BV2 cells. The results of the present study indicated that hesperetin inhibited BV2 cell pyroptosis and significantly blocked the expression of NLRP3 inflammasome proteins (NLRP3 Caspase-1 p10 apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain [ASC]) and pro-inflammatory mediators (IL-18, IL-1β). Furthermore, the silencing of Nrf2 by small interfering ribonucleic acid (siRNA) partially abolished its antioxidant effect in the aforementioned cell experiments. 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Liu, Zhongyuan |
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Liu, Zhongyuan ddc 610 fid PHARM bkl 44.38 misc Hesperetin misc Neuroinflammation misc Oxidative stress misc Nrf2 signaling pathway misc NLRP3-mediated pyroptosis Hesperetin ameliorates spinal cord injury by inhibiting NLRP3 inflammasome activation and pyroptosis through enhancing Nrf2 signaling |
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610 DE-600 PHARM DE-84 fid 44.38 bkl Hesperetin ameliorates spinal cord injury by inhibiting NLRP3 inflammasome activation and pyroptosis through enhancing Nrf2 signaling Hesperetin Neuroinflammation Oxidative stress Nrf2 signaling pathway NLRP3-mediated pyroptosis |
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Hesperetin ameliorates spinal cord injury by inhibiting NLRP3 inflammasome activation and pyroptosis through enhancing Nrf2 signaling |
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Hesperetin ameliorates spinal cord injury by inhibiting NLRP3 inflammasome activation and pyroptosis through enhancing Nrf2 signaling |
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Liu, Zhongyuan Tu, Kewu Zou, Peiqian Liao, Congrui Ding, Ruoting Huang, Zucheng Huang, Zhiping Yao, Xinqiang Chen, Jianting Zhang, Zhongmin |
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hesperetin ameliorates spinal cord injury by inhibiting nlrp3 inflammasome activation and pyroptosis through enhancing nrf2 signaling |
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Hesperetin ameliorates spinal cord injury by inhibiting NLRP3 inflammasome activation and pyroptosis through enhancing Nrf2 signaling |
| abstract |
Neuroinflammation is a prominent feature of traumatic spinal cord injuries (SCIs). Hesperetin exhibits anti-inflammatory effects in neurological disorders; however, the potential neuroprotective effects of hesperetin in cases of SCI remain unclear. Sprague-Dawley rats with C5 hemi-contusion injuries were used as an SCI model. Hesperetin was administered to the experimental rats in order to investigate its neuroprotective effects after SCI, and BV2 cells were pretreated with hesperetin or silencing of nuclear factor erythroid 2-related factor 2 (siNrf2), and then stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). The therapeutic impact and molecular mechanism of hesperetin were elucidated in a series of in vivo and in vitro investigations conducted using a combination of experiments. The results of the present in vivo experiment indicated that hesperetin improved functional recovery and protected spinal cord tissue after SCI. Hesperetin attenuated oxidative stress and microglial activation, lowered malondialdehyde (MDA) levels, and elevated catalase (CAT), glutathione (GSH)-Px, and superoxide dismutase (SOD) levels. Moreover, hesperetin downregulated the expression of advanced oxygenation protein products (AOPPs), ionized calcium-binding adapter molecule 1 (Iba-1), NOD-like receptor protein 3 (NLRP3), and interleukin-1 beta (IL-1β), but increased the expression of Nrf2. In vitro studies have shown that hesperetin inhibits the generation of reactive oxygen species (ROS), as well as the neuroinflammation associated with the upregulation of Nrf2 and heme oxygenase-1 (HO-1) in BV2 cells. The results of the present study indicated that hesperetin inhibited BV2 cell pyroptosis and significantly blocked the expression of NLRP3 inflammasome proteins (NLRP3 Caspase-1 p10 apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain [ASC]) and pro-inflammatory mediators (IL-18, IL-1β). Furthermore, the silencing of Nrf2 by small interfering ribonucleic acid (siRNA) partially abolished its antioxidant effect in the aforementioned cell experiments. Collectively, these findings illustrate that through an increase in Nrf2 signaling hesperetin reduces oxidative stress and neuroinflammation by suppressing NLRP3 inflammasome activation and pyroptosis. |
| abstractGer |
Neuroinflammation is a prominent feature of traumatic spinal cord injuries (SCIs). Hesperetin exhibits anti-inflammatory effects in neurological disorders; however, the potential neuroprotective effects of hesperetin in cases of SCI remain unclear. Sprague-Dawley rats with C5 hemi-contusion injuries were used as an SCI model. Hesperetin was administered to the experimental rats in order to investigate its neuroprotective effects after SCI, and BV2 cells were pretreated with hesperetin or silencing of nuclear factor erythroid 2-related factor 2 (siNrf2), and then stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). The therapeutic impact and molecular mechanism of hesperetin were elucidated in a series of in vivo and in vitro investigations conducted using a combination of experiments. The results of the present in vivo experiment indicated that hesperetin improved functional recovery and protected spinal cord tissue after SCI. Hesperetin attenuated oxidative stress and microglial activation, lowered malondialdehyde (MDA) levels, and elevated catalase (CAT), glutathione (GSH)-Px, and superoxide dismutase (SOD) levels. Moreover, hesperetin downregulated the expression of advanced oxygenation protein products (AOPPs), ionized calcium-binding adapter molecule 1 (Iba-1), NOD-like receptor protein 3 (NLRP3), and interleukin-1 beta (IL-1β), but increased the expression of Nrf2. In vitro studies have shown that hesperetin inhibits the generation of reactive oxygen species (ROS), as well as the neuroinflammation associated with the upregulation of Nrf2 and heme oxygenase-1 (HO-1) in BV2 cells. The results of the present study indicated that hesperetin inhibited BV2 cell pyroptosis and significantly blocked the expression of NLRP3 inflammasome proteins (NLRP3 Caspase-1 p10 apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain [ASC]) and pro-inflammatory mediators (IL-18, IL-1β). Furthermore, the silencing of Nrf2 by small interfering ribonucleic acid (siRNA) partially abolished its antioxidant effect in the aforementioned cell experiments. Collectively, these findings illustrate that through an increase in Nrf2 signaling hesperetin reduces oxidative stress and neuroinflammation by suppressing NLRP3 inflammasome activation and pyroptosis. |
| abstract_unstemmed |
Neuroinflammation is a prominent feature of traumatic spinal cord injuries (SCIs). Hesperetin exhibits anti-inflammatory effects in neurological disorders; however, the potential neuroprotective effects of hesperetin in cases of SCI remain unclear. Sprague-Dawley rats with C5 hemi-contusion injuries were used as an SCI model. Hesperetin was administered to the experimental rats in order to investigate its neuroprotective effects after SCI, and BV2 cells were pretreated with hesperetin or silencing of nuclear factor erythroid 2-related factor 2 (siNrf2), and then stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). The therapeutic impact and molecular mechanism of hesperetin were elucidated in a series of in vivo and in vitro investigations conducted using a combination of experiments. The results of the present in vivo experiment indicated that hesperetin improved functional recovery and protected spinal cord tissue after SCI. Hesperetin attenuated oxidative stress and microglial activation, lowered malondialdehyde (MDA) levels, and elevated catalase (CAT), glutathione (GSH)-Px, and superoxide dismutase (SOD) levels. Moreover, hesperetin downregulated the expression of advanced oxygenation protein products (AOPPs), ionized calcium-binding adapter molecule 1 (Iba-1), NOD-like receptor protein 3 (NLRP3), and interleukin-1 beta (IL-1β), but increased the expression of Nrf2. In vitro studies have shown that hesperetin inhibits the generation of reactive oxygen species (ROS), as well as the neuroinflammation associated with the upregulation of Nrf2 and heme oxygenase-1 (HO-1) in BV2 cells. The results of the present study indicated that hesperetin inhibited BV2 cell pyroptosis and significantly blocked the expression of NLRP3 inflammasome proteins (NLRP3 Caspase-1 p10 apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain [ASC]) and pro-inflammatory mediators (IL-18, IL-1β). Furthermore, the silencing of Nrf2 by small interfering ribonucleic acid (siRNA) partially abolished its antioxidant effect in the aforementioned cell experiments. Collectively, these findings illustrate that through an increase in Nrf2 signaling hesperetin reduces oxidative stress and neuroinflammation by suppressing NLRP3 inflammasome activation and pyroptosis. |
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Tu, Kewu Zou, Peiqian Liao, Congrui Ding, Ruoting Huang, Zucheng Huang, Zhiping Yao, Xinqiang Chen, Jianting Zhang, Zhongmin |
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Tu, Kewu Zou, Peiqian Liao, Congrui Ding, Ruoting Huang, Zucheng Huang, Zhiping Yao, Xinqiang Chen, Jianting Zhang, Zhongmin |
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2024-07-06T23:34:49.537Z |
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