| Literature DB >> 26113037 |
Can Wei1, Yan Zhao2, Lina Wang1, Xue Peng1, Hong Li1, Yajun Zhao1, Yuqin He1, Hongjiang Shao1, Xin Zhong1,3, Hongzhu Li1,3, Changqing Xu1,3.
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.Entities:
Keywords: aged hearts; cardiomyocytes; hydrogen sulfide; post-conditioning
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Year: 2015 PMID: 26113037 DOI: 10.1002/cbin.10507
Source DB: PubMed Journal: Cell Biol Int ISSN: 1065-6995 Impact factor: 3.612