Research Article
Effect of eNOS on Ischemic Postconditioning-Induced Autophagy against Ischemia/Reperfusion Injury in Mice
Figure 6
HPostC attenuated H9c2 cells H/R injury via activating AMPK/eNOS-mediated autophagy. (a), (b) HPostC increased the ratio of LC3-II/LC3-I and decreased p62 expression, which was abolished by the eNOS inhibitor L-NIO. (c), (d) eNOS siRNA abolished the effects of HPostC on the ratio of LC3-II/LC3-I and p62 expression. (e) HPostC increased the phosphorylation of eNOS. The AMPK inhibitor Compound C abolished the effect of HPostC on eNOS. (f) HPostC increased the expression of p-ANPK compared to H/R group, and Compound C decreased the phosphorylation of AMPK. n=3 per group. , versus Control; versus H/R; versus HPostC.
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