Open Access<p>Dexmedetomidine Attenuates Cellular Injury and Apoptosis in H9c2 Cardiomyocytes by Regulating p-38MAPK and Endoplasmic Reticulum Stress</p>
Author(s) -
Zhipeng Zhu,
Xiaoyan Ling,
Hongmei Zhou,
Caijun Zhang,
Weiwei Yan
Publication year - 2020
Publication title -
drug design, development and therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.964
H-Index - 64
ISSN - 1177-8881
DOI - 10.2147/dddt.s265970
Subject(s) - endoplasmic reticulum , thapsigargin , chop , apoptosis , lactate dehydrogenase , viability assay , cardioprotection , unfolded protein response , p38 mitogen activated protein kinases , chemistry , flow cytometry , reperfusion injury , pharmacology , microbiology and biotechnology , medicine , endocrinology , mapk/erk pathway , biology , signal transduction , ischemia , immunology , biochemistry , enzyme
Myocardial ischaemia-reperfusion injury (IRI) has been confirmed to induce endoplasmic reticulum stress (ERS) when myocardial cell function continues to deteriorate to a certain degree. The clinical applications of effective tested strategies are sometimes inconsistent with the applications evaluated in experiments, although reasonable mechanisms and diverse signalling pathways have been broadly explored. Dexmedetomidine (DEX) has been shown to attenuate IRI of the heart in animal studies. This study aimed to determine whether DEX can protect injured cardiomyocytes under hypoxia/reoxygenation (H/R) at the cellular level and whether the mechanism is related to ERS and the p38 MAPK pathway.