Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1

Context Pterostilbene (PTE), a common polyphenol compound, exerts an anti-inflammatory effect in many diseases, including acute lung injury (ALI).Objective This study explores the potential mechanism of PTE pre-treatment against lipopolysaccharide (LPS)-induced ALI.Materials and methods Sixty Spragu...
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Autor*in:	Ying Li [verfasserIn] Shu-Min Wang [verfasserIn] Xing Li [verfasserIn] Chang-Jun Lv [verfasserIn] Ling-Yun Peng [verfasserIn] Xiao-Feng Yu [verfasserIn] Ying-Jian Song [verfasserIn] Cong-Jie Wang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	Lipopolysaccharide-induced nuclear factor-κB pathway inflammatory cells inflammatory factors

Übergeordnetes Werk:	In: Pharmaceutical Biology - Taylor & Francis Group, 2017, 60(2022), 1, Seite 394-403
Übergeordnetes Werk:	volume:60 ; year:2022 ; number:1 ; pages:394-403

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1080/13880209.2022.2034893

Katalog-ID:	DOAJ016044010

Internformat


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245	1	0	\|a Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1
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520			\|a Context Pterostilbene (PTE), a common polyphenol compound, exerts an anti-inflammatory effect in many diseases, including acute lung injury (ALI).Objective This study explores the potential mechanism of PTE pre-treatment against lipopolysaccharide (LPS)-induced ALI.Materials and methods Sixty Sprague-Dawley rats were divided into control, ALI, 10 mg/kg PTE + LPS, 20 mg/kg PTE + LPS, and 40 mg/kg PTE + LPS groups. At 24 h before LPS instillation, PTE was administered orally. At 2 h before LPS instillation, PTE was again administered orally. After 24 h of LPS treatment, the rats were euthanized. The levels of inflammatory cells and inflammatory factors in the bronchoalveolar lavage fluid (BALF), the expression of nuclear receptor subfamily 4 group A member 1 (NR4A1), and the nuclear factor (NF)-κB pathway-related protein levels were detected. NR4A1 agonist was used to further investigate the mechanism of PTE pre-treatment.Results After PTE pre-treatment, the LPS induced inflammation was controlled and the survival rate was increased to 100% from 70% after LPS treatment 24 h. For lung injury score, it decreased to 1.5 from 3.5 after treating 40 mg/kg PTE. Compared with the control group, the expression of NR4A1 in the ALI group was decreased by 20–40%. However, the 40 mg/kg PTE pre-treatment increased the NR4A1 expression by 20–40% in the lung tissue. The results obtained with pre-treatment NR4A1 agonist were similar to those obtained by pre-treatment 40 mg/kg PTE.Conclusions PTE pre-treatment might represent an appropriate therapeutic target and strategy for preventing ALI induced by LPS.
650		4	\|a Lipopolysaccharide-induced
650		4	\|a nuclear factor-κB pathway
650		4	\|a inflammatory cells
650		4	\|a inflammatory factors
653		0	\|a Therapeutics. Pharmacology
700	0		\|a Shu-Min Wang \|e verfasserin \|4 aut
700	0		\|a Xing Li \|e verfasserin \|4 aut
700	0		\|a Chang-Jun Lv \|e verfasserin \|4 aut
700	0		\|a Ling-Yun Peng \|e verfasserin \|4 aut
700	0		\|a Xiao-Feng Yu \|e verfasserin \|4 aut
700	0		\|a Ying-Jian Song \|e verfasserin \|4 aut
700	0		\|a Cong-Jie Wang \|e verfasserin \|4 aut
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allfields	10.1080/13880209.2022.2034893 doi (DE-627)DOAJ016044010 (DE-599)DOAJ690a6d20be64472b9304e757ce817249 DE-627 ger DE-627 rakwb eng RM1-950 Ying Li verfasserin aut Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Context Pterostilbene (PTE), a common polyphenol compound, exerts an anti-inflammatory effect in many diseases, including acute lung injury (ALI).Objective This study explores the potential mechanism of PTE pre-treatment against lipopolysaccharide (LPS)-induced ALI.Materials and methods Sixty Sprague-Dawley rats were divided into control, ALI, 10 mg/kg PTE + LPS, 20 mg/kg PTE + LPS, and 40 mg/kg PTE + LPS groups. At 24 h before LPS instillation, PTE was administered orally. At 2 h before LPS instillation, PTE was again administered orally. After 24 h of LPS treatment, the rats were euthanized. The levels of inflammatory cells and inflammatory factors in the bronchoalveolar lavage fluid (BALF), the expression of nuclear receptor subfamily 4 group A member 1 (NR4A1), and the nuclear factor (NF)-κB pathway-related protein levels were detected. NR4A1 agonist was used to further investigate the mechanism of PTE pre-treatment.Results After PTE pre-treatment, the LPS induced inflammation was controlled and the survival rate was increased to 100% from 70% after LPS treatment 24 h. For lung injury score, it decreased to 1.5 from 3.5 after treating 40 mg/kg PTE. Compared with the control group, the expression of NR4A1 in the ALI group was decreased by 20–40%. However, the 40 mg/kg PTE pre-treatment increased the NR4A1 expression by 20–40% in the lung tissue. The results obtained with pre-treatment NR4A1 agonist were similar to those obtained by pre-treatment 40 mg/kg PTE.Conclusions PTE pre-treatment might represent an appropriate therapeutic target and strategy for preventing ALI induced by LPS. Lipopolysaccharide-induced nuclear factor-κB pathway inflammatory cells inflammatory factors Therapeutics. Pharmacology Shu-Min Wang verfasserin aut Xing Li verfasserin aut Chang-Jun Lv verfasserin aut Ling-Yun Peng verfasserin aut Xiao-Feng Yu verfasserin aut Ying-Jian Song verfasserin aut Cong-Jie Wang verfasserin aut In Pharmaceutical Biology Taylor & Francis Group, 2017 60(2022), 1, Seite 394-403 (DE-627)300595905 (DE-600)1483151-X 17445116 nnns volume:60 year:2022 number:1 pages:394-403 https://doi.org/10.1080/13880209.2022.2034893 kostenfrei https://doaj.org/article/690a6d20be64472b9304e757ce817249 kostenfrei https://www.tandfonline.com/doi/10.1080/13880209.2022.2034893 kostenfrei https://doaj.org/toc/1388-0209 Journal toc kostenfrei https://doaj.org/toc/1744-5116 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 60 2022 1 394-403
spelling	10.1080/13880209.2022.2034893 doi (DE-627)DOAJ016044010 (DE-599)DOAJ690a6d20be64472b9304e757ce817249 DE-627 ger DE-627 rakwb eng RM1-950 Ying Li verfasserin aut Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Context Pterostilbene (PTE), a common polyphenol compound, exerts an anti-inflammatory effect in many diseases, including acute lung injury (ALI).Objective This study explores the potential mechanism of PTE pre-treatment against lipopolysaccharide (LPS)-induced ALI.Materials and methods Sixty Sprague-Dawley rats were divided into control, ALI, 10 mg/kg PTE + LPS, 20 mg/kg PTE + LPS, and 40 mg/kg PTE + LPS groups. At 24 h before LPS instillation, PTE was administered orally. At 2 h before LPS instillation, PTE was again administered orally. After 24 h of LPS treatment, the rats were euthanized. The levels of inflammatory cells and inflammatory factors in the bronchoalveolar lavage fluid (BALF), the expression of nuclear receptor subfamily 4 group A member 1 (NR4A1), and the nuclear factor (NF)-κB pathway-related protein levels were detected. NR4A1 agonist was used to further investigate the mechanism of PTE pre-treatment.Results After PTE pre-treatment, the LPS induced inflammation was controlled and the survival rate was increased to 100% from 70% after LPS treatment 24 h. For lung injury score, it decreased to 1.5 from 3.5 after treating 40 mg/kg PTE. Compared with the control group, the expression of NR4A1 in the ALI group was decreased by 20–40%. However, the 40 mg/kg PTE pre-treatment increased the NR4A1 expression by 20–40% in the lung tissue. The results obtained with pre-treatment NR4A1 agonist were similar to those obtained by pre-treatment 40 mg/kg PTE.Conclusions PTE pre-treatment might represent an appropriate therapeutic target and strategy for preventing ALI induced by LPS. Lipopolysaccharide-induced nuclear factor-κB pathway inflammatory cells inflammatory factors Therapeutics. Pharmacology Shu-Min Wang verfasserin aut Xing Li verfasserin aut Chang-Jun Lv verfasserin aut Ling-Yun Peng verfasserin aut Xiao-Feng Yu verfasserin aut Ying-Jian Song verfasserin aut Cong-Jie Wang verfasserin aut In Pharmaceutical Biology Taylor & Francis Group, 2017 60(2022), 1, Seite 394-403 (DE-627)300595905 (DE-600)1483151-X 17445116 nnns volume:60 year:2022 number:1 pages:394-403 https://doi.org/10.1080/13880209.2022.2034893 kostenfrei https://doaj.org/article/690a6d20be64472b9304e757ce817249 kostenfrei https://www.tandfonline.com/doi/10.1080/13880209.2022.2034893 kostenfrei https://doaj.org/toc/1388-0209 Journal toc kostenfrei https://doaj.org/toc/1744-5116 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 60 2022 1 394-403
allfields_unstemmed	10.1080/13880209.2022.2034893 doi (DE-627)DOAJ016044010 (DE-599)DOAJ690a6d20be64472b9304e757ce817249 DE-627 ger DE-627 rakwb eng RM1-950 Ying Li verfasserin aut Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Context Pterostilbene (PTE), a common polyphenol compound, exerts an anti-inflammatory effect in many diseases, including acute lung injury (ALI).Objective This study explores the potential mechanism of PTE pre-treatment against lipopolysaccharide (LPS)-induced ALI.Materials and methods Sixty Sprague-Dawley rats were divided into control, ALI, 10 mg/kg PTE + LPS, 20 mg/kg PTE + LPS, and 40 mg/kg PTE + LPS groups. At 24 h before LPS instillation, PTE was administered orally. At 2 h before LPS instillation, PTE was again administered orally. After 24 h of LPS treatment, the rats were euthanized. The levels of inflammatory cells and inflammatory factors in the bronchoalveolar lavage fluid (BALF), the expression of nuclear receptor subfamily 4 group A member 1 (NR4A1), and the nuclear factor (NF)-κB pathway-related protein levels were detected. NR4A1 agonist was used to further investigate the mechanism of PTE pre-treatment.Results After PTE pre-treatment, the LPS induced inflammation was controlled and the survival rate was increased to 100% from 70% after LPS treatment 24 h. For lung injury score, it decreased to 1.5 from 3.5 after treating 40 mg/kg PTE. Compared with the control group, the expression of NR4A1 in the ALI group was decreased by 20–40%. However, the 40 mg/kg PTE pre-treatment increased the NR4A1 expression by 20–40% in the lung tissue. The results obtained with pre-treatment NR4A1 agonist were similar to those obtained by pre-treatment 40 mg/kg PTE.Conclusions PTE pre-treatment might represent an appropriate therapeutic target and strategy for preventing ALI induced by LPS. Lipopolysaccharide-induced nuclear factor-κB pathway inflammatory cells inflammatory factors Therapeutics. Pharmacology Shu-Min Wang verfasserin aut Xing Li verfasserin aut Chang-Jun Lv verfasserin aut Ling-Yun Peng verfasserin aut Xiao-Feng Yu verfasserin aut Ying-Jian Song verfasserin aut Cong-Jie Wang verfasserin aut In Pharmaceutical Biology Taylor & Francis Group, 2017 60(2022), 1, Seite 394-403 (DE-627)300595905 (DE-600)1483151-X 17445116 nnns volume:60 year:2022 number:1 pages:394-403 https://doi.org/10.1080/13880209.2022.2034893 kostenfrei https://doaj.org/article/690a6d20be64472b9304e757ce817249 kostenfrei https://www.tandfonline.com/doi/10.1080/13880209.2022.2034893 kostenfrei https://doaj.org/toc/1388-0209 Journal toc kostenfrei https://doaj.org/toc/1744-5116 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 60 2022 1 394-403
allfieldsGer	10.1080/13880209.2022.2034893 doi (DE-627)DOAJ016044010 (DE-599)DOAJ690a6d20be64472b9304e757ce817249 DE-627 ger DE-627 rakwb eng RM1-950 Ying Li verfasserin aut Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Context Pterostilbene (PTE), a common polyphenol compound, exerts an anti-inflammatory effect in many diseases, including acute lung injury (ALI).Objective This study explores the potential mechanism of PTE pre-treatment against lipopolysaccharide (LPS)-induced ALI.Materials and methods Sixty Sprague-Dawley rats were divided into control, ALI, 10 mg/kg PTE + LPS, 20 mg/kg PTE + LPS, and 40 mg/kg PTE + LPS groups. At 24 h before LPS instillation, PTE was administered orally. At 2 h before LPS instillation, PTE was again administered orally. After 24 h of LPS treatment, the rats were euthanized. The levels of inflammatory cells and inflammatory factors in the bronchoalveolar lavage fluid (BALF), the expression of nuclear receptor subfamily 4 group A member 1 (NR4A1), and the nuclear factor (NF)-κB pathway-related protein levels were detected. NR4A1 agonist was used to further investigate the mechanism of PTE pre-treatment.Results After PTE pre-treatment, the LPS induced inflammation was controlled and the survival rate was increased to 100% from 70% after LPS treatment 24 h. For lung injury score, it decreased to 1.5 from 3.5 after treating 40 mg/kg PTE. Compared with the control group, the expression of NR4A1 in the ALI group was decreased by 20–40%. However, the 40 mg/kg PTE pre-treatment increased the NR4A1 expression by 20–40% in the lung tissue. The results obtained with pre-treatment NR4A1 agonist were similar to those obtained by pre-treatment 40 mg/kg PTE.Conclusions PTE pre-treatment might represent an appropriate therapeutic target and strategy for preventing ALI induced by LPS. Lipopolysaccharide-induced nuclear factor-κB pathway inflammatory cells inflammatory factors Therapeutics. Pharmacology Shu-Min Wang verfasserin aut Xing Li verfasserin aut Chang-Jun Lv verfasserin aut Ling-Yun Peng verfasserin aut Xiao-Feng Yu verfasserin aut Ying-Jian Song verfasserin aut Cong-Jie Wang verfasserin aut In Pharmaceutical Biology Taylor & Francis Group, 2017 60(2022), 1, Seite 394-403 (DE-627)300595905 (DE-600)1483151-X 17445116 nnns volume:60 year:2022 number:1 pages:394-403 https://doi.org/10.1080/13880209.2022.2034893 kostenfrei https://doaj.org/article/690a6d20be64472b9304e757ce817249 kostenfrei https://www.tandfonline.com/doi/10.1080/13880209.2022.2034893 kostenfrei https://doaj.org/toc/1388-0209 Journal toc kostenfrei https://doaj.org/toc/1744-5116 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 60 2022 1 394-403
allfieldsSound	10.1080/13880209.2022.2034893 doi (DE-627)DOAJ016044010 (DE-599)DOAJ690a6d20be64472b9304e757ce817249 DE-627 ger DE-627 rakwb eng RM1-950 Ying Li verfasserin aut Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Context Pterostilbene (PTE), a common polyphenol compound, exerts an anti-inflammatory effect in many diseases, including acute lung injury (ALI).Objective This study explores the potential mechanism of PTE pre-treatment against lipopolysaccharide (LPS)-induced ALI.Materials and methods Sixty Sprague-Dawley rats were divided into control, ALI, 10 mg/kg PTE + LPS, 20 mg/kg PTE + LPS, and 40 mg/kg PTE + LPS groups. At 24 h before LPS instillation, PTE was administered orally. At 2 h before LPS instillation, PTE was again administered orally. After 24 h of LPS treatment, the rats were euthanized. The levels of inflammatory cells and inflammatory factors in the bronchoalveolar lavage fluid (BALF), the expression of nuclear receptor subfamily 4 group A member 1 (NR4A1), and the nuclear factor (NF)-κB pathway-related protein levels were detected. NR4A1 agonist was used to further investigate the mechanism of PTE pre-treatment.Results After PTE pre-treatment, the LPS induced inflammation was controlled and the survival rate was increased to 100% from 70% after LPS treatment 24 h. For lung injury score, it decreased to 1.5 from 3.5 after treating 40 mg/kg PTE. Compared with the control group, the expression of NR4A1 in the ALI group was decreased by 20–40%. However, the 40 mg/kg PTE pre-treatment increased the NR4A1 expression by 20–40% in the lung tissue. The results obtained with pre-treatment NR4A1 agonist were similar to those obtained by pre-treatment 40 mg/kg PTE.Conclusions PTE pre-treatment might represent an appropriate therapeutic target and strategy for preventing ALI induced by LPS. Lipopolysaccharide-induced nuclear factor-κB pathway inflammatory cells inflammatory factors Therapeutics. Pharmacology Shu-Min Wang verfasserin aut Xing Li verfasserin aut Chang-Jun Lv verfasserin aut Ling-Yun Peng verfasserin aut Xiao-Feng Yu verfasserin aut Ying-Jian Song verfasserin aut Cong-Jie Wang verfasserin aut In Pharmaceutical Biology Taylor & Francis Group, 2017 60(2022), 1, Seite 394-403 (DE-627)300595905 (DE-600)1483151-X 17445116 nnns volume:60 year:2022 number:1 pages:394-403 https://doi.org/10.1080/13880209.2022.2034893 kostenfrei https://doaj.org/article/690a6d20be64472b9304e757ce817249 kostenfrei https://www.tandfonline.com/doi/10.1080/13880209.2022.2034893 kostenfrei https://doaj.org/toc/1388-0209 Journal toc kostenfrei https://doaj.org/toc/1744-5116 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 60 2022 1 394-403
language	English
source	In Pharmaceutical Biology 60(2022), 1, Seite 394-403 volume:60 year:2022 number:1 pages:394-403
sourceStr	In Pharmaceutical Biology 60(2022), 1, Seite 394-403 volume:60 year:2022 number:1 pages:394-403
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Lipopolysaccharide-induced nuclear factor-κB pathway inflammatory cells inflammatory factors Therapeutics. Pharmacology
isfreeaccess_bool	true
container_title	Pharmaceutical Biology
authorswithroles_txt_mv	Ying Li @@aut@@ Shu-Min Wang @@aut@@ Xing Li @@aut@@ Chang-Jun Lv @@aut@@ Ling-Yun Peng @@aut@@ Xiao-Feng Yu @@aut@@ Ying-Jian Song @@aut@@ Cong-Jie Wang @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	300595905
id	DOAJ016044010
language_de	englisch
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At 24 h before LPS instillation, PTE was administered orally. At 2 h before LPS instillation, PTE was again administered orally. After 24 h of LPS treatment, the rats were euthanized. The levels of inflammatory cells and inflammatory factors in the bronchoalveolar lavage fluid (BALF), the expression of nuclear receptor subfamily 4 group A member 1 (NR4A1), and the nuclear factor (NF)-κB pathway-related protein levels were detected. NR4A1 agonist was used to further investigate the mechanism of PTE pre-treatment.Results After PTE pre-treatment, the LPS induced inflammation was controlled and the survival rate was increased to 100% from 70% after LPS treatment 24 h. For lung injury score, it decreased to 1.5 from 3.5 after treating 40 mg/kg PTE. Compared with the control group, the expression of NR4A1 in the ALI group was decreased by 20–40%. However, the 40 mg/kg PTE pre-treatment increased the NR4A1 expression by 20–40% in the lung tissue. The results obtained with pre-treatment NR4A1 agonist were similar to those obtained by pre-treatment 40 mg/kg PTE.Conclusions PTE pre-treatment might represent an appropriate therapeutic target and strategy for preventing ALI induced by LPS.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Lipopolysaccharide-induced</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">nuclear factor-κB pathway</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">inflammatory cells</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">inflammatory factors</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Therapeutics. 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callnumber-first	R - Medicine
author	Ying Li
spellingShingle	Ying Li misc RM1-950 misc Lipopolysaccharide-induced misc nuclear factor-κB pathway misc inflammatory cells misc inflammatory factors misc Therapeutics. Pharmacology Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1
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topic_title	RM1-950 Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1 Lipopolysaccharide-induced nuclear factor-κB pathway inflammatory cells inflammatory factors
topic	misc RM1-950 misc Lipopolysaccharide-induced misc nuclear factor-κB pathway misc inflammatory cells misc inflammatory factors misc Therapeutics. Pharmacology
topic_unstemmed	misc RM1-950 misc Lipopolysaccharide-induced misc nuclear factor-κB pathway misc inflammatory cells misc inflammatory factors misc Therapeutics. Pharmacology
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title	Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1
ctrlnum	(DE-627)DOAJ016044010 (DE-599)DOAJ690a6d20be64472b9304e757ce817249
title_full	Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1
author_sort	Ying Li
journal	Pharmaceutical Biology
journalStr	Pharmaceutical Biology
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lang_code	eng
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publishDateSort	2022
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author_browse	Ying Li Shu-Min Wang Xing Li Chang-Jun Lv Ling-Yun Peng Xiao-Feng Yu Ying-Jian Song Cong-Jie Wang
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format_se	Elektronische Aufsätze
author-letter	Ying Li
doi_str_mv	10.1080/13880209.2022.2034893
author2-role	verfasserin
title_sort	pterostilbene pre-treatment reduces lps-induced acute lung injury through activating nr4a1
callnumber	RM1-950
title_auth	Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1
abstract	Context Pterostilbene (PTE), a common polyphenol compound, exerts an anti-inflammatory effect in many diseases, including acute lung injury (ALI).Objective This study explores the potential mechanism of PTE pre-treatment against lipopolysaccharide (LPS)-induced ALI.Materials and methods Sixty Sprague-Dawley rats were divided into control, ALI, 10 mg/kg PTE + LPS, 20 mg/kg PTE + LPS, and 40 mg/kg PTE + LPS groups. At 24 h before LPS instillation, PTE was administered orally. At 2 h before LPS instillation, PTE was again administered orally. After 24 h of LPS treatment, the rats were euthanized. The levels of inflammatory cells and inflammatory factors in the bronchoalveolar lavage fluid (BALF), the expression of nuclear receptor subfamily 4 group A member 1 (NR4A1), and the nuclear factor (NF)-κB pathway-related protein levels were detected. NR4A1 agonist was used to further investigate the mechanism of PTE pre-treatment.Results After PTE pre-treatment, the LPS induced inflammation was controlled and the survival rate was increased to 100% from 70% after LPS treatment 24 h. For lung injury score, it decreased to 1.5 from 3.5 after treating 40 mg/kg PTE. Compared with the control group, the expression of NR4A1 in the ALI group was decreased by 20–40%. However, the 40 mg/kg PTE pre-treatment increased the NR4A1 expression by 20–40% in the lung tissue. The results obtained with pre-treatment NR4A1 agonist were similar to those obtained by pre-treatment 40 mg/kg PTE.Conclusions PTE pre-treatment might represent an appropriate therapeutic target and strategy for preventing ALI induced by LPS.
abstractGer	Context Pterostilbene (PTE), a common polyphenol compound, exerts an anti-inflammatory effect in many diseases, including acute lung injury (ALI).Objective This study explores the potential mechanism of PTE pre-treatment against lipopolysaccharide (LPS)-induced ALI.Materials and methods Sixty Sprague-Dawley rats were divided into control, ALI, 10 mg/kg PTE + LPS, 20 mg/kg PTE + LPS, and 40 mg/kg PTE + LPS groups. At 24 h before LPS instillation, PTE was administered orally. At 2 h before LPS instillation, PTE was again administered orally. After 24 h of LPS treatment, the rats were euthanized. The levels of inflammatory cells and inflammatory factors in the bronchoalveolar lavage fluid (BALF), the expression of nuclear receptor subfamily 4 group A member 1 (NR4A1), and the nuclear factor (NF)-κB pathway-related protein levels were detected. NR4A1 agonist was used to further investigate the mechanism of PTE pre-treatment.Results After PTE pre-treatment, the LPS induced inflammation was controlled and the survival rate was increased to 100% from 70% after LPS treatment 24 h. For lung injury score, it decreased to 1.5 from 3.5 after treating 40 mg/kg PTE. Compared with the control group, the expression of NR4A1 in the ALI group was decreased by 20–40%. However, the 40 mg/kg PTE pre-treatment increased the NR4A1 expression by 20–40% in the lung tissue. The results obtained with pre-treatment NR4A1 agonist were similar to those obtained by pre-treatment 40 mg/kg PTE.Conclusions PTE pre-treatment might represent an appropriate therapeutic target and strategy for preventing ALI induced by LPS.
abstract_unstemmed	Context Pterostilbene (PTE), a common polyphenol compound, exerts an anti-inflammatory effect in many diseases, including acute lung injury (ALI).Objective This study explores the potential mechanism of PTE pre-treatment against lipopolysaccharide (LPS)-induced ALI.Materials and methods Sixty Sprague-Dawley rats were divided into control, ALI, 10 mg/kg PTE + LPS, 20 mg/kg PTE + LPS, and 40 mg/kg PTE + LPS groups. At 24 h before LPS instillation, PTE was administered orally. At 2 h before LPS instillation, PTE was again administered orally. After 24 h of LPS treatment, the rats were euthanized. The levels of inflammatory cells and inflammatory factors in the bronchoalveolar lavage fluid (BALF), the expression of nuclear receptor subfamily 4 group A member 1 (NR4A1), and the nuclear factor (NF)-κB pathway-related protein levels were detected. NR4A1 agonist was used to further investigate the mechanism of PTE pre-treatment.Results After PTE pre-treatment, the LPS induced inflammation was controlled and the survival rate was increased to 100% from 70% after LPS treatment 24 h. For lung injury score, it decreased to 1.5 from 3.5 after treating 40 mg/kg PTE. Compared with the control group, the expression of NR4A1 in the ALI group was decreased by 20–40%. However, the 40 mg/kg PTE pre-treatment increased the NR4A1 expression by 20–40% in the lung tissue. The results obtained with pre-treatment NR4A1 agonist were similar to those obtained by pre-treatment 40 mg/kg PTE.Conclusions PTE pre-treatment might represent an appropriate therapeutic target and strategy for preventing ALI induced by LPS.
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container_issue	1
title_short	Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1
url	https://doi.org/10.1080/13880209.2022.2034893 https://doaj.org/article/690a6d20be64472b9304e757ce817249 https://www.tandfonline.com/doi/10.1080/13880209.2022.2034893 https://doaj.org/toc/1388-0209 https://doaj.org/toc/1744-5116
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author2	Shu-Min Wang Xing Li Chang-Jun Lv Ling-Yun Peng Xiao-Feng Yu Ying-Jian Song Cong-Jie Wang
author2Str	Shu-Min Wang Xing Li Chang-Jun Lv Ling-Yun Peng Xiao-Feng Yu Ying-Jian Song Cong-Jie Wang
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up_date	2024-07-03T18:39:13.443Z
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Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1

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