Abstract:OBJECTIVE To investigate the protective effect of honokiol on oxidative stress injury of cardiomyocytes induced by high fat and its correlation with AMP-activated protein kinase(AMPK) signaling pathway. METHODS The lipotoxic injury model of cardiomyocyte was established by palmitic acid (PA). The proliferation of cardiomyocyte was evaluated by MTT assay after pretreatment with honokiol. The oxidative stress and apoptotic level of cardiomyocyte were measured by kit. The expression of AMPK pathway and apoptotic pathway-related protein was evaluated by Western blotting. RESULTS PA (0.4 mmol·L-1) stimulation for 24 and 48 h could significantly reduce the cell proliferation ability, and a model of cardiac myocyte lipid toxicity injury was successfully established. The high-fat stimulation condition was set as PA (0.4 mmol·L-1) stimulation for 24 h, and could significantly increase the level of reactive oxygen species (ROS) in cells and promote cell death. The expression levels of p-AMPK protein and anti-apoptotic protein Bcl-2 were decreased, and the expression levels of p-p70S6K, apoptotic protein Bax and cleaved caspase 3 were increased. Pretreatment with honokiol could significantly reverse the above changes. CONCLUSION Honokiol has significant protective effect on lipid toxicity of cardiac myocytes, and its mechanism is related to the reversal of oxidative stress injury mediated by AMPK pathway.
黄家喜, 李晶, 鲍翠玉. 和厚朴酚对棕榈酸诱导的心肌细胞毒性保护作用及机制研究[J]. 中国药学杂志, 2021, 56(4): 293-298.
HUANG Jia-xi, LI Jing, BAO Cui-yu. Protective Effects of Honokiol on Lipid-Induced Cardiomyocyte Injury and Its Mechanism. Chinese Pharmaceutical Journal, 2021, 56(4): 293-298.
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