In order to investigate miR-4763-3p and associated genes’ roles in myocarditis, AC16 cell line was divided into LPS + miR-4763-3p inhibitor, LPS + NC inhibitor, LPS + miR-4763-3p inhibitor + si-IL10RA and NC groups, and Q-PCR was used to find out whether miR-4763-3p was expressed; Targetscan, Genecards, and MiRDB were used to estimate the miR-4763-3p target; Targetscan was used to display binding sites. Western blot assay was undertaken to detect Bax, Bcl-2, and IL10RA expression. Proliferation and apoptosis were processed using CCK8 and the flow cytometry assay, respectively. Migration and invasion were confirmed utilizing Transwell test. ELISA assay was processed to show the content of IL-6, IL-1ß, IL-10 and TGF-ß in the cell culture supernatant. After being exposed to LPS, cardiomyocyte cells expressed more miR-4763-3p. MiR-4763-3p inhibitor accelerated proliferation, migration and invasion behavior, while it also decreased apoptosis rate in LPS-treated cardiomyocyte cells. MiR-4763-3p inhibitor attenuated the inflammatory response by up-regulating Bax expression and down-regulating Bcl-2 level in LPS-treated cardiomyocyte cells. In cardiomyocyte cells treated with LPS, MiR-4763-3p expression was elevated. si-IL10RA The miR-4763-3p inhibitor restored its effects. MiR-4763-3p accelerates lipopolysaccharide-induced cardiomyocyte apoptosis and inflammatory response by targeting IL10RA, which might be a potential target for myocarditis.

为了研究miR-4763-3p及相关基因在心肌炎中的作用，将AC16细胞系分为LPS+miR-4763-3p抑制剂、LPS+NC抑制剂、LPS+miR-4763-3p抑制剂+si-IL10RA和NC组，Q-PCR检测miR-4763-3p是否表达；Targetscan、Genecards 和 MiRDB 用于估计 miR-4763-3p 靶标；Targetscan 用于显示结合位点。采用蛋白质印迹法检测 Bax、Bcl-2 和 IL10RA 的表达。分别使用CCK8和流式细胞术测定处理增殖和凋亡。利用Transwell测试证实迁移和侵袭。进行ELISA测定以显示细胞培养上清液中IL-6、IL-1β、IL-10和TGF-β的含量。暴露于 LPS 后，心肌细胞表达更多的 miR-4763-3p。MiR-4763-3p抑制剂加速了LPS处理的心肌细胞的增殖、迁移和侵袭行为，同时也降低了细胞凋亡率。MiR-4763-3p 抑制剂通过上调 LPS 处理的心肌细胞中的 Bax 表达和下调 Bcl-2 水平来减弱炎症反应。在用 LPS 处理的心肌细胞中，MiR-4763-3p 表达升高。si-IL10RA miR-4763-3p 抑制剂恢复了其作用。MiR-4763-3p 通过靶向 IL10RA 加速脂多糖诱导的心肌细胞凋亡和炎症反应，IL10RA 可能是心肌炎的潜在靶点。