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Hydrogen Sulfide Ameliorates Ischemia/Reperfusion-Induced Hepatitis by Inhibiting Apoptosis and Autophagy Pathways
Background. Hepatic ischemia/reperfusion (I/R) injury is an important clinical problem, and its consequences can seriously threaten human health. Apoptosis and autophagy have been shown to contribute to cell death in hepatic I/R injury. Hydrogen sulfide (H(2)S) is the third most common endogenously...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4055384/ https://www.ncbi.nlm.nih.gov/pubmed/24966472 http://dx.doi.org/10.1155/2014/935251 |
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author | Cheng, Ping Wang, Fan Chen, Kan Shen, Miao Dai, Weiqi Xu, Ling Zhang, Yan Wang, Chengfen Li, Jingjing Yang, Jing Zhu, Rong Zhang, Huawei Zheng, Yuanyuan Lu, Jie Zhou, Yingqun Guo, Chuanyong |
author_facet | Cheng, Ping Wang, Fan Chen, Kan Shen, Miao Dai, Weiqi Xu, Ling Zhang, Yan Wang, Chengfen Li, Jingjing Yang, Jing Zhu, Rong Zhang, Huawei Zheng, Yuanyuan Lu, Jie Zhou, Yingqun Guo, Chuanyong |
author_sort | Cheng, Ping |
collection | PubMed |
description | Background. Hepatic ischemia/reperfusion (I/R) injury is an important clinical problem, and its consequences can seriously threaten human health. Apoptosis and autophagy have been shown to contribute to cell death in hepatic I/R injury. Hydrogen sulfide (H(2)S) is the third most common endogenously produced gaseous signaling molecule and is known to exert a protective effect against hepatic I/R injury. In this study, the purpose is to explore both the effect and mechanism of H(2)S on hepatic I/R injury. Methods. Balb/c mice were randomized into Sham, I/R, or two doses (14 μmol/kg and 28 μmol/kg) of sodium hydrosulfide (NaHS, an H(2)S donor) preconditioning groups. Results. NaHS significantly reduced the levels of TNF-α and IL-6 at 12 h and 24 h after injection compared with ischemia/reperfusion challenge alone. The expression of Bcl-2, Bax, Beclin-1, and LC3, which play important roles in the regulation of the apoptosis and autophagy pathways, was also clearly affected by NaHS. Furthermore, NaHS affected the p-JNK1, p-ERK1, and p-p38. Conclusion. Our results indicate that H(2)S attenuates hepatic I/R injury, at least in part, by regulating apoptosis through inhibiting JNK1 signaling. The autophagy agonist rapamycin potentiated this hepatoprotective effect by reversing the inhibition of autophagy by H(2)S. |
format | Online Article Text |
id | pubmed-4055384 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-40553842014-06-25 Hydrogen Sulfide Ameliorates Ischemia/Reperfusion-Induced Hepatitis by Inhibiting Apoptosis and Autophagy Pathways Cheng, Ping Wang, Fan Chen, Kan Shen, Miao Dai, Weiqi Xu, Ling Zhang, Yan Wang, Chengfen Li, Jingjing Yang, Jing Zhu, Rong Zhang, Huawei Zheng, Yuanyuan Lu, Jie Zhou, Yingqun Guo, Chuanyong Mediators Inflamm Research Article Background. Hepatic ischemia/reperfusion (I/R) injury is an important clinical problem, and its consequences can seriously threaten human health. Apoptosis and autophagy have been shown to contribute to cell death in hepatic I/R injury. Hydrogen sulfide (H(2)S) is the third most common endogenously produced gaseous signaling molecule and is known to exert a protective effect against hepatic I/R injury. In this study, the purpose is to explore both the effect and mechanism of H(2)S on hepatic I/R injury. Methods. Balb/c mice were randomized into Sham, I/R, or two doses (14 μmol/kg and 28 μmol/kg) of sodium hydrosulfide (NaHS, an H(2)S donor) preconditioning groups. Results. NaHS significantly reduced the levels of TNF-α and IL-6 at 12 h and 24 h after injection compared with ischemia/reperfusion challenge alone. The expression of Bcl-2, Bax, Beclin-1, and LC3, which play important roles in the regulation of the apoptosis and autophagy pathways, was also clearly affected by NaHS. Furthermore, NaHS affected the p-JNK1, p-ERK1, and p-p38. Conclusion. Our results indicate that H(2)S attenuates hepatic I/R injury, at least in part, by regulating apoptosis through inhibiting JNK1 signaling. The autophagy agonist rapamycin potentiated this hepatoprotective effect by reversing the inhibition of autophagy by H(2)S. Hindawi Publishing Corporation 2014 2014-05-21 /pmc/articles/PMC4055384/ /pubmed/24966472 http://dx.doi.org/10.1155/2014/935251 Text en Copyright © 2014 Ping Cheng et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Cheng, Ping Wang, Fan Chen, Kan Shen, Miao Dai, Weiqi Xu, Ling Zhang, Yan Wang, Chengfen Li, Jingjing Yang, Jing Zhu, Rong Zhang, Huawei Zheng, Yuanyuan Lu, Jie Zhou, Yingqun Guo, Chuanyong Hydrogen Sulfide Ameliorates Ischemia/Reperfusion-Induced Hepatitis by Inhibiting Apoptosis and Autophagy Pathways |
title | Hydrogen Sulfide Ameliorates Ischemia/Reperfusion-Induced Hepatitis by Inhibiting Apoptosis and Autophagy Pathways |
title_full | Hydrogen Sulfide Ameliorates Ischemia/Reperfusion-Induced Hepatitis by Inhibiting Apoptosis and Autophagy Pathways |
title_fullStr | Hydrogen Sulfide Ameliorates Ischemia/Reperfusion-Induced Hepatitis by Inhibiting Apoptosis and Autophagy Pathways |
title_full_unstemmed | Hydrogen Sulfide Ameliorates Ischemia/Reperfusion-Induced Hepatitis by Inhibiting Apoptosis and Autophagy Pathways |
title_short | Hydrogen Sulfide Ameliorates Ischemia/Reperfusion-Induced Hepatitis by Inhibiting Apoptosis and Autophagy Pathways |
title_sort | hydrogen sulfide ameliorates ischemia/reperfusion-induced hepatitis by inhibiting apoptosis and autophagy pathways |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4055384/ https://www.ncbi.nlm.nih.gov/pubmed/24966472 http://dx.doi.org/10.1155/2014/935251 |
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