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Methylamine irisolidone, a novel compound, increases total ATPase activity and inhibits apoptosis in vivo and in vitro
- Yin, Mao-Shan, Xu, Shu-Hong, Wang, Yan, Jie, Li, Zhang, Qiang, Zheng, Wu-Mei, Sun, Xiao-Hui, Liang, Chen, Wang, Fu-Wen, Xi, Xiao-Hui, Mu, Yan-Ling
- Journal of Asian natural products research 2016 v.18 no.6 pp. 562-575
- adenosinetriphosphatase, animal models, apoptosis, cardiac output, caspase-9, cell viability, hypoxia, in vitro studies, membrane potential, methylamine, mitochondrial membrane, myocardial ischemia, myocardium, protective effect, rats, reactive oxygen species, sodium, staining, surgery
- We propose to further research the protective effect of MMI on myocardium ischemic rat model and H9c2 cells that underwent cell apoptosis induced by hypoxia. We established the myocardium ischemic rat model via the cardiac surgical procedures in vivo and treated the model rats with different concentration of MMI. In vitro , with the pretreatment of MMI for 12 h in the model of Na ₂S ₂O ₄-induced hypoxia injury, the H9c2 cells viability was determined by MTT assay. We found that MMI had significantly improved cardiac function of the myocardial ischemia, and significantly decreased the reactive oxygen species level. The expression of P53, Bcl-2, Bax, and caspase-9 was also induced by MMI. In vitro study revealed a concentration-dependent increase in cell viability associated with MMI pretreatment. Annexin V-FITC and PI staining results showed that MMI had a preventive effect on hypoxia-induced apoptosis in H9c2 cells. MMI also inhibited the mitochondrial membrane potential decrease and increased total ATPase activity during hypoxia in H9c2 cells. In conclusion, MMI can enhance the cardiac function in myocardial ischemic rat and increase cell viability and attenuate the apoptosis in H9c2 cells induced by hypoxia, which was associated with inhibiting MMP decreasion and increasing total ATPase activity.