Hydrogen Sulfide Ameliorates Ischemia/Reperfusion-Induced Hepatitis by Inhibiting Apoptosis and Autophagy Pathways
Figure 9
In the condition of hepatic ischemia-reperfusion injury, H2S reduces autophagy (which is an important protective mechanism against I/R- and A/R-induced hepatitis) through the suppression of the JNK pathway. However, it also plays an antiapoptotic role in ameliorating I/R- and A/R-induced hepatitis and these protective effects are enhanced by the inhibition of JNK. Our findings show that, although autophagy was inhibited by H2S, H2S still showed a protective effect against I/R. Furthermore, the JNK1-mediated phosphorylation of Bcl-2 substantially reduced the affinity of Bcl-2 for Beclin-1, leading to its rapid dissociation from Beclin-1 and the subsequent induction of prosurvival autophagy, reducing hepatic I/R injury. In our study, the reduced phosphorylation of JNK1 (compared with that in the I/R and A/R groups) by preconditioning with NaHS may have weakened the process described above.
