Aconitine Induces Myocardial Damage in Rats Associated With Activation of the JNK1/2 Signaling Pathway

Acute Aconitine (Acon) poisoning can cause arrhythmia and myocardial damage; however, the underlying mechanisms remain unclear. This study investigated the mechanism of myocardial injury induced by acute Acon poisoning. A rat model (n = 51) of acute Acon poisoning was established by intragastric administration. Electrocardiographic tracings were used to record changes in cardiac rhythm. Hematoxylin and eosin (HE) staining and Masson staining were performed to evaluate myocardial pathological injury and collagen deposition. The expression levels of cardiac enzymes and proteins in venous blood were detected using enzyme-linked immunosorbent assay (ELISA) kits. The structure-activity relationship between Acon and the JNK pathway was investigated by molecular docking. The expression levels of phosphorylated c-Jun N-terminal kinase 1/2 (JNK1/2) proteins were detected by Western blotting. In this study, ventricular arrhythmias were observed in rats following intragastric administration of Acon. Myocardial tissue showed a disordered arrangement of myocardial fibers and cells, accompanied by abnormal collagen deposition. Molecular docking results indicated potential interactions between Acon and JNK1/2. Meanwhile, the expression levels of cardiac enzymes and proteins, as well as phosphorylated JNK1/2, were significantly increased. Further studies demonstrated that treatment with the JNK inhibitor SP600125 partially reversed Acon-induced myocardial injury in rats. These results indicate that JNK1/2 phosphorylation is involved in the development of myocardial injury induced by acute Aconitine poisoning. The findings suggest that activation of the JNK1/2 signaling pathway contributes to Aconitine-induced myocardial damage, and that inhibition of the JNK1/2 pathway may alleviate myocardial injury caused by acute Aconitine intoxication.