急性心肌梗死(AMI)是由缺血和缺氧引起的最严重的冠心病。该研究旨在研究神经肽的作用以及电针(EA)在急性心肌梗死(AMI)治疗中的作用。与正常人群相比,在AMI患者的血清中观察到P物质(SP)的显着增加。在SP处理的AMI小鼠模型中PGI2表达增加,TXA2表达降低。和PI3K通路相关基因,包括Pik3ca,Akt,而Mtor,在SP治疗的AMI患者的心肌组织中上调。用SP处理的人心肌细胞系(HCM)增加了PI3K途径相关基因的mRNA和蛋白表达(Pik3ca,Pik3cb,Akt,和Mtor)。与MI对照和EA治疗的MI大鼠模型相比,Myd88,MTOR,Akt1,Sp,和Irak1差异表达,与体内和体外研究一致。根据京都基因和基因组百科全书(KEGG),EA处理显著富集MI相关差异表达基因(DEGs)内的PI3K/AKT信号通路基因。此外,通过分子对接分析证实,PIK3CA,AKT1和mTOR与神经肽SP形成稳定的对接。PI3K/AKT通路活性可通过SP直接或间接受到EA的影响,这纠正了AMI中PGI2/TXA2代谢失衡。作为这一发现的结果,现在更好地理解MI治疗。
Acute myocardial infarction (AMI) is the most severe form of coronary heart disease caused by ischemia and hypoxia. The study is aimed at investigating the role of neuropeptides and the mechanism of electroacupuncture (EA) in acute myocardial infarction (AMI) treatment. Compared with the normal population, a significant increase in substance P (SP) was observed in the serum of patients with AMI. PGI2 expression was increased in the SP-treated AMI mouse model, and TXA2 expression was decreased. And PI3K pathway-related genes, including Pik3ca, Akt, and Mtor, were upregulated in myocardial tissue of SP-treated AMI patients. Human cardiomyocyte cell lines (HCM) treated with SP increased mRNA and protein expression of PI3K pathway-related genes (Pik3ca, Pik3cb, Akt, and Mtor). Compared to MI control and EA-treated MI rat models, Myd88, MTOR, Akt1, Sp, and Irak1 were differentially expressed, consistent with in vivo and in vitro studies. EA treatment significantly enriched PI3K/AKT signaling pathway genes within MI-associated differentially expressed genes (DEGs) according to Kyoto Encyclopedia of Genes and Genomes (KEGG). Furthermore, it was confirmed by molecular docking analysis that PIK3CA, AKT1, and mTOR form stable dockings with neuropeptide SP. PI3K/AKT pathway activity may be affected directly or indirectly by EA via SP, which corrects the PGI2/TXA2 metabolic imbalance in AMI. MI treatment is now better understood as a result of this finding.