Methylamine irisolidone, a novel compound, increases total ATPase activity and inhibits apoptosis in vivo and in vitro.

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 Na2S2O4-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.

Protective effect of methylamine irisolidone on cardiac function in rats with acute myocardial infarction / 中国药学杂志

OBJECTIVE: To observe the effect of a new compound methylamine irisolidone on cardiac function in rats with experiment myocardial infarction. METHODS: The male Wistar rats were randomly divided into 6 groups: control group, ischemia model group, methylamine irisolidone preconditioning group, pretreated with different dosages of methylamine irisolidone (200,100,50 mg · kg-1, respectively) and 200 mg · kg-1 puerain(positive control). Coronary artery ligation was used to induce the acute myocardial ischemia model. After 30 d administration of methylamine irisolidone, the heart function parameters,including heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), left ventricular systolic pressure (LVSP), maximal velocity of increase and decrease of left ventriclar pressure (dp/dtmax), were analyzed and myocardial histology was analyzed by hematoxylin-eosin staining. RESULTS: Compared with model group, methylamine irisolidone could improve the heart function of rats in AMI injury, increased the systolic pressure and diastolic pressure, decreased the heart rate(P < 0.01). The myocardial ultrastructure injury was alleviate. CONCLUSION: Methylamine irisolidone had cardioprotective effects on acute myocardial ischemia. The mechanism may be related to slow down heart rate, prolong diastolic, so that an increase in the endocardial blood supply.