1. Effect and mechanism of gomisin D on the isoproterenol induced myocardial injury in H9C2 cells and mice.
- Author
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Chen, Zi-Han, Liu, Yan-Xin, Chen, Zhi-Wei, Lin, Mo-Di, Zhang, Jin-Lan, Wang, Zhe, and Sun, Hua
- Subjects
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MYOCARDIAL infarction , *BIOLOGICAL models , *IN vitro studies , *MITOCHONDRIA , *T-test (Statistics) , *STATISTICAL significance , *RESEARCH funding , *APOPTOSIS , *OXIDATIVE stress , *PEPTIDE hormones , *IN vivo studies , *DESCRIPTIVE statistics , *ISOPROTERENOL , *CELL lines , *MICE , *REACTIVE oxygen species , *HYPERTROPHY , *CREATINE kinase , *ISOENZYMES , *CALCIUM , *ENERGY metabolism , *MEDICINAL plants , *ANIMAL experimentation , *MOLECULAR structure , *MYOCARDIUM , *ATRIAL natriuretic peptides , *ONE-way analysis of variance , *DATA analysis software , *HEART cells - Abstract
We established myocardial injury models in vivo and in vitro to investigate the cardioprotective effect of gomisin D obtained from Schisandra chinensis. Gomisin D significantly inhibited isoproterenol-induced apoptosis and hypertrophy in H9C2 cells. Gomisin D decreased serum BNP, ANP, CK-MB, cTn-T levels and histopathological alterations, and inhibited myocardial hypertrophy in mice. In mechanisms research, gomisin D reversed ISO-induced accumulation of intracellular ROS and Ca2+. Gomisin D further improved mitochondrial energy metabolism disorders by regulating the TCA cycle. These results demonstrated that gomisin D had a significant effect on isoproterenol-induced myocardial injury by inhibiting oxidative stress, calcium overload and improving mitochondrial energy metabolism. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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