Sodium Aescinate Protects Myocardial Injury Induced by Methylparathion Poisoning by Regulating The miR-301/Rock1 Axis

Abstract

Methylparathion is a highly toxic insecticide known to cause lung, liver, and myocardial injuries, could lead to myocardial injury. These injuries are known to be ameliorated by sodium aescinate. In this study, we have examined the mechanism of diminution of sodium aescinate-mediated myocardial injury. To this end, we have examined the biochemical changes in the heart muscles isolated from rats, and in rat heart myoblast cell, H9c2. Both rats and H9c2 cells were treated with methylparathion followed by increasing dosage of sodium aescinate. Data from quantitative reverse transcription polymerase chain reaction or Western blot analyses show that miR-301 expression was decreased, while Rock1 was increased, in methylparathion-induced heart tissues or H9c2 cells. Treatment with sodium aescinate increased miR-301 expression and decreased Rock1 expression in a dosage-dependent manner. MicroRNAs bind to the 3′ - untranslated region of the target gene leading to the degradation of target mRNA. Methylparathion treatment reduced miR-301 expression in H9c2 cells, while increased Rock1 expression. However, sodium aescinate treatment enhanced miR-301 expression and repress Rock1 expression in a dosage-dependent manner. Methylparathion reduces cell viability of H9c2, while promotes the cell apoptosis. However, treatment with sodium aescinate rescues from methylparathion-induced cytotoxicity, while forced Rock1 expression aggravates methylparathion-induced cytotoxicity. In conclusion, sodium aescinate amelioration of methylparathion-induced myocardial injury by miR-301/Rock1 axis provides a new therapeutic strategy for the management of methylparathion poisoning.