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We observed that ischemia\/reperfusion (I\/R) inhibited the phosphorylation of extracellular signal\u2010regulated kinase 1\/2 (ERK1\/2) and promoted phosphorylation of p38 MAPK and c\u2010Jun N\u2010terminal kinase (JNK) in both young hearts and aged hearts. PC up\u2010regulated ERK1\/2 phosphorylations and down\u2010regulated p38 MAPK and JNK phosphorylations. Exogenous H<jats:sub>2<\/jats:sub>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\u2010treatment with exogenous H<jats:sub>2<\/jats:sub>S\u2010induced ERK1\/2 and reduced p38 MAPK and JNK phosphorylations. These results suggest that exogenous H<jats:sub>2<\/jats:sub>S recovers PC\u2010induced cardioprotection via MAPK pathway in the aged hearts.<\/jats:p><\/jats:sec>","DOI":"10.1002\/cbin.10507","type":"journal-article","created":{"date-parts":[[2015,6,26]],"date-time":"2015-06-26T05:07:01Z","timestamp":1435295221000},"page":"1173-1176","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["H<sub>2<\/sub>S restores the cardioprotection from ischemic post\u2010conditioning in isolated aged rat hearts"],"prefix":"10.1002","volume":"39","author":[{"given":"Can","family":"Wei","sequence":"first","affiliation":[{"name":"Department of Pathophysiology Harbin Medical University Baojian Road Harbin 150081 China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of emergency the Second Affiliated Hospital of Harbin Medical University Harbin 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