• Changgan Mo, Hui Han, Xiuge Tang, Xinxu Lu, Yin Wei, Dan Luo, and Zhuodong Zhou.
• Department of Cardiology, The First Affiliated Hospital of Jinan University, Guangzhou, China.
• Panminerva Med. 2023 Sep 1; 65 (3): 343350343-350.

BackgroundThe aim of this study was to study the effect of protein kinase TBK1 and IKKε inhibitor Amlexanox on cardiac function after acute myocardial infarction (AMI) in rats.MethodsAMI model was established in rats. Experimental grouping: sham + dimethyl sulfoxide (DMSO) group, sham + Amlexanox group, AMI + DMSO group, AMI + Amlexanox group. 12 h after surgery, rats in the sham + Amlexanox group and AMI + Amlexanox group were given an intraperitoneal injection of Amlexanox at a dose of 25 mg/kg once a day for 7 consecutive days. The sham + DMSO group and the AMI + DMSO group were given the same amount of DMSO as a control. Ultrasound was used to detect changes in cardiac function in rats for 3 and 7 days after continuous administration, and real-time polymerase chain reaction was used to detect the transcription levels of ISGs and apoptosis in myocardial tissue. Hematoxylin-eosin and immunohistochemical staining were used to observe the inflammatory cell infiltration level and MOMA2 expression in myocardial tissue. Western blot was used to examine the TBK1 signaling pathway and its downstream protein expression.ResultsAmlexanox can improve left ventricular ejection fraction (LVEF) and short-axis shortening rate (FS) after AMI in rats, reduce remodeling of cardiomyopathy, and reduce inflammatory cell infiltration, thus reducing myocardial apoptosis.ConclusionsThe protein kinases TBK1 and IKKε inhibitor Amlexanox can improve cardiac function in rats after AMI, reduce myocardial inflammatory response, reduce myocardial apoptosis, and then exert myocardial protection in vivo.

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