Hydrogen Sulfide Ameliorates IschemiaReperfusion-Induced Hepatitis by Inhibiting Apoptosis and Autophagy Pathways

Abstract EN

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 (H2S) 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 H2S 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 H2S 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 H2S 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 H2S.