Effect and mechanism of gomisin D on the isoproterenol induced myocardial injury in H9C2 cells and mice.
| Autor: | Chen, Zi-Han, Liu, Yan-Xin, Chen, Zhi-Wei, Lin, Mo-Di, Zhang, Jin-Lan, Wang, Zhe, Sun, Hua |
|---|---|
| Předmět: |
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 |
| Zdroj: | Journal of Asian Natural Products Research; May2024, Vol. 26 Issue 5, p604-615, 12p |
| Abstrakt: | 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] |
| Databáze: | Complementary Index |
| Externí odkaz: |
|