{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T20:57:01Z","timestamp":1783457821343,"version":"3.55.0"},"reference-count":40,"publisher":"Canadian Science Publishing","issue":"2","license":[{"start":{"date-parts":[[2022,2,1]],"date-time":"2022-02-01T00:00:00Z","timestamp":1643673600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[2022,2]]},"abstract":"<jats:p> Myocardial ischemia\/reperfusion (I\/R) injury causes irreversible injury to the heart, thereby causing acute myocardial infarction. Midazolam is a benzodiazepine commonly utilized in anesthesia and intensive care. Research has indicated that midazolam plays a critical role in many diseases; however, the function of midazolam in myocardial injury induced by I\/R still needs further investigation. The infarct size and damage to the heart tissues were examined through 2,3,5-triphenyl tetrazolium chloride (TTC) staining and hematoxylin and eosin staining. The creatine kinase-myocardial band isoenzyme, lactate dehydrogenase, and aspartate aminotransferase levels were tested using commercial kits. Cell apoptosis was determined through TUNEL staining or flow cytometry assays. Bax, Bcl-2, cleaved caspase-3, phospho-38 (p-p38), p38, p-JNK, JNK, extracellular signal-regulated kinases (ERK), and p-ERK expression was examined through Western blot. In our study, midazolam was shown to suppress the infarct size and heart tissue damage and reduce myocardial enzyme leakage in I\/R rats. Additionally, midazolam was found to retard cardiomyocyte apoptosis in I\/R rats. The JNK\/p38 MAPK signaling pathway in I\/R rats was inhibited by midazolam. Our findings demonstrated that in hypoxia\/reoxygenation (H\/R) \u2013 mediated H9C2 cells, anisomycin abolished the suppressive effects of midazolam on the JNK\/p38 MAPK signaling pathway. Next, exploration discovered that anisomycin abolished the cytoprotective effects of midazolam on H\/R-treated H9C2 cell apoptosis. In conclusion, this work demonstrated that midazolam retarded I\/R-induced cardiomyocyte apoptosis by inhibiting the JNK\/p38 MAPK signaling pathway. These results may provide new insight into the treatment of myocardial I\/R injury. <\/jats:p>","DOI":"10.1139\/cjpp-2021-0289","type":"journal-article","created":{"date-parts":[[2021,9,24]],"date-time":"2021-09-24T21:37:41Z","timestamp":1632519461000},"page":"117-124","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":16,"title":["Midazolam suppresses ischemia\/reperfusion-induced cardiomyocyte apoptosis by inhibiting the JNK\/p38 MAPK signaling pathway"],"prefix":"10.1139","volume":"100","author":[{"given":"Weixiao","family":"Zhou","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, Zhuji People\u2019s Hospital of Zhejiang Province, Zhuji Affiliated Hospital of Wenzhou Medical University, Zhuji, Zhejiang 311800, China."},{"name":"Department of Anesthesiology, Zhuji People\u2019s Hospital of Zhejiang Province, Zhuji Affiliated Hospital of Wenzhou Medical University, Zhuji, Zhejiang 311800, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dongjiang","family":"Cai","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Zhuji People\u2019s Hospital of Zhejiang Province, Zhuji Affiliated Hospital of Wenzhou Medical University, Zhuji, Zhejiang 311800, China."},{"name":"Department of Anesthesiology, Zhuji People\u2019s Hospital of Zhejiang Province, Zhuji Affiliated Hospital of Wenzhou Medical University, Zhuji, Zhejiang 311800, China."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"155","reference":[{"key":"refg1\/ref1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2006.04.013"},{"key":"refg2\/ref2","doi-asserted-by":"publisher","DOI":"10.1016\/j.mcna.2007.03.005"},{"key":"refg3\/ref3","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbalip.2018.02.003"},{"key":"refg4\/ref4","doi-asserted-by":"publisher","DOI":"10.1111\/jcmm.13584"},{"key":"refg5\/ref5","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00022.2018"},{"key":"refg6\/ref6","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2019.09.001"},{"key":"refg7\/ref7","doi-asserted-by":"publisher","DOI":"10.7326\/L19-0603"},{"key":"refg8\/ref8","doi-asserted-by":"publisher","DOI":"10.2165\/00003495-199244030-00002"},{"key":"refg9\/ref9","first-page":"117","volume":"7","author":"Harada H.","year":"2003","journal-title":"Rev. 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