Role of hydrogen sulfide in hepatic ischemia-reperfusion–induced injury in rats

✍ Scribed by Kai Kang; Mingyan Zhao; Hongchi Jiang; Gang Tan; Shangha Pan; Xueying Sun

• Publisher: John Wiley and Sons
• Year: 2009
• Tongue: English
• Weight: 410 KB
• Volume: 15
• Category: Article
• ISSN: 1527-6465
• DOI: 10.1002/lt.21810

✦ Synopsis

Hydrogen sulfide (H 2 S) displays anti-inflammatory and cytoprotective activities as evidenced by the inhibition of myocardial ischemia-reperfusion injury and production of lipid peroxidation. H 2 S also exerts many physiological or pathological effects on livers. Therefore, we designed the present study to investigate the roles of H 2 S in hepatic ischemia-reperfusion (HIR)-induced injury in rats by measuring H 2 S levels, H 2 S synthesizing activity, and cystathionine ␥-lyase (CSE) messenger RNA (mRNA) expression. We also applied DL-propargyl glycine (PAG) and sodium hydrosulfide (NaHS) to investigate their effects on the severity of liver injury induced by HIR. The levels of H 2 S, H 2 S production activity, and CSE mRNA expression in livers were increased by HIR. Administration of NaHS significantly attenuated the severity of liver injury and inhibited the production of lipid peroxidation, serum inflammatory factors [including nitric oxide, tumor necrosis factor ␣ (TNF-␣), interleukin 10, and intercellular cell adhesion molecule 1], cell apoptosis, and apoptosis-related proteins (including caspase-3, Fas, Fas ligand, and TNF-␣), which were caused or elevated by HIR, whereas PAG aggravated them. However, NaHS or PAG did not show significant effects on the activation of caspase-9, which was also increased by HIR. Although further investigation is required, this study may indicate that H 2 S plays a protective role in HIR-induced injury.