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Non‐esterified fatty acids induce apoptosis via a ROS‐dependent mechanism involving the mitochondrial pathway in bovine abomasal smooth muscle cells
Author(s) -
Wei Teng,
Tian Wulin,
Xie Guanghong
Publication year - 2014
Publication title -
european journal of lipid science and technology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.614
H-Index - 94
eISSN - 1438-9312
pISSN - 1438-7697
DOI - 10.1002/ejlt.201400137
Subject(s) - nefa , apoptosis , cytochrome c , fatty acid , chemistry , viability assay , oxidative stress , biochemistry , oleic acid
Increased blood non‐esterified fatty acid (NEFA) concentrations might be implicated as a factor that plays a role in the pathogenesis of gastrointestinal motility disorder, such as abomasal displacement. We sought to elucidate possible effects of high concentrations of NEFA on primary cultured bovine abomasal smooth muscle cells (BSMC). BSMC treated with high concentrations of NEFA resulted in decrease of cell viability and increase of cell apoptosis rate. NEFA treatment induced oxidative stress, as revealed by increased levels of ROS and MDA, while decreased the antioxidative abilities (SOD, CAT, GSH, and GSSG) in BSMC. Meanwhile, high concentrations of NEFA induced BSMC mitochondrial apoptotic cell death. Mitochondrial membrane potential decrease, increased Bax and decreased Bcl‐2, cytochrome c release, caspases activation, and apoptosis inducing factor (AIF) translocation were observed in NEFA‐treated cells. Pretreatment with the antioxidant N ‐acetylcysteine (NAC) effectively reversed these NEFA‐induced events. In conclusion, these results show that NEFA induce BSMC apoptosis mainly via a ROS‐dependent mechanism involving the mitochondrial pathway. The cytotoxicity of non‐esterified fatty acid (consist of oleic acid, linoleic acid, palmitic acid, stearic acid, and palmitoleic acid) on primary cultured bovine abomasal smooth muscle cell, and the underlying molecular mechanism.