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Acetylcholine Attenuated TNF-α-Induced Apoptosis in H9c2 Cells: Role of Calpain and the p38-MAPK Pathway
Author(s) -
Ming Zhao,
Yang Yang,
XueYuan Bi,
XiaoJiang Yu,
Hang-Huan Jia,
Huanle Fang,
Weijin Zang
Publication year - 2015
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000430157
Subject(s) - calpastatin , calpain , p38 mitogen activated protein kinases , microbiology and biotechnology , apoptosis , mapk/erk pathway , tumor necrosis factor alpha , chemistry , caspase , phosphorylation , biology , programmed cell death , endocrinology , biochemistry , enzyme
Previous studies have shown that inflammation is associated with excessive activation of calpains. Acetylcholine (ACh) has been reported to inhibit pro-inflammatory cytokine release and protect against cardiomyocyte injury. However, there is no direct evidence regarding whether ACh can regulate calpains to exert cardioprotection. To this end, we investigated the effect of ACh on tumour necrosis factor alpha (TNF-α)-induced cardiomyocyte injury and further explored the underlying mechanism.

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