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Abstract Background Aconitine (Acon) poisoning can cause arrhythmia and myocardial damage, but the specific mechanism of myocardial damage caused by acon poisoning is still unclear. This study explored the mechanism of myocardial damage caused by acute acon poisoning by constructing a rat acuteacon poisoning model. Methods First, the rats were divided into 4 groups (n = 9): control group, Acet group, Acon-1 mg group, and Acon-2 mg group (Detect 3 rats in each group at 1/2/3 h; 36 rats in total), When conducted the second part of the experiment to examine the role of the JNK pathway in acon poisoning, the rats were divided into 5 groups (n=3): control group, Acon-2 mg group, DMSO group, Acon-2 mg+SP600125 group, and Acon-2 mg+Anis group (15 rats in total). Rat model of acute acon poisoning was constructed by intragastric administration. Electrocardiogram tracings were used to record rat heart rhythm changes, and H myocardial collagen hyperplasia is abnormal, and myocardial fibrosis occurs. At the same time, the expression levels of cardiac enzymes and cardiac proteins in venous blood increased. In addition, JNK1/2 phosphorylation levels increased. Further study showed that use of a JNK inhibitor (SP600125) partially reversed Acon's damage to rat myocardium. Conclusions Taken together, these results indicate that JNK1 / 2 phosphorylation is involved in the development of myocardial damage induced by acute Acon poisoning. In addition, the intervention effect of JNK specific inhibitor on myocardial damage induced by acute Acon poisoning was obvious, which may provide new insights into the important role of inhibiting the JNK1/2 pathway in alleviating myocardial damage caused by acute Acon intoxication.
Hu et al. (Tue,) studied this question.
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