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Updated: Apr 8, 2026

Induction and Assessment of Ischemia-reperfusion Injury in Langendorff-perfused Rat Hearts
Published on: July 27, 2015
H2 S restores the cardioprotection from ischemic post-conditioning in isolated aged rat hearts
Can Wei1, Yan Zhao2, Lina Wang1
1Department of Pathophysiology, Harbin Medical University, Baojian Road, Harbin, 150081, China.
Abstract:
This study explored the mechanisms underlying the recovery of myocardial protection from ischemic post-conditioning (PC) by exogenous hydrogen sulfide (H2 S) in aged rat hearts. We observed that ischemia/reperfusion (I/R) inhibited the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and promoted phosphorylation of p38 MAPK and c-Jun N-terminal kinase (JNK) in both young hearts and aged hearts. PC up-regulated ERK1/2 phosphorylations and down-regulated p38 MAPK and JNK phosphorylations. Exogenous H2 S further enhanced the role of PC in the young hearts. In the aged hearts, PC failed to affect all these 3 MAPK members, while co-treatment with exogenous H2 S-induced ERK1/2 and reduced p38 MAPK and JNK phosphorylations. These results suggest that exogenous H2 S recovers PC-induced cardioprotection via MAPK pathway in the aged hearts.

