Qianfu Wu1,2, Haihui Wang1, Fei He3, Jiali Zheng2, Hongjing Zhang4, Chang Cheng5, Panwei Hu2, Rong Lu6,7, Guoliang Yan1,2. 1. Department of Geriatrics, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200071, China. 2. Department of Pathology, School of Basic Medical Sciences, Shanghai University of Traditional Chinese Medicine, No. 1200, Cailun, Pudong New Area, Shanghai, 201203, China. 3. Department of Cardiology, Second Affiliated Hospital of Anhui Medical University, Hefei, 230601, Anhui, China. 4. Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200437, China. 5. Department of Nuclear Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, 200030, Shanghai, China. 6. Department of Geriatrics, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200071, China. lurong@shutcm.edu.cn. 7. Department of Pathology, School of Basic Medical Sciences, Shanghai University of Traditional Chinese Medicine, No. 1200, Cailun, Pudong New Area, Shanghai, 201203, China. lurong@shutcm.edu.cn.
Abstract
OBJECTIVE: As some articles have highlighted the role of microRNA-92a (miR-92a) in myocardial ischemia-reperfusion injury (MI/RI), this article aimed to investigate the effect of miR-92a on Sevoflurane (Sevo)-treated MI/RI via regulation of Krüppel-like factor 4 (KLF4). METHODS: An MI/RI rat model was established by ligating the left anterior descending coronary artery. The cardiac function, pathological changes of myocardial tissues, inflammatory response, oxidative stress and cardiomyocyte apoptosis in MI/RI rats were determined. KLF4 and miR-92a expression was detected in the myocardial tissue of rats, and the target relationship between miR-92a and KLF4 was confirmed. RESULTS: Sevo treatment alleviated myocardial damage, inflammatory response, oxidative stress response, and cardiomyocyte apoptosis, and improved cardiac function in MI/RI rats. miR-92a increased and KLF4 decreased in the myocardial tissue of MI/RI rats. KLF4 was targeted by miR-92a. Downregulation of miR-92a or upregulation of KLF4 further enhanced the effect of Sevo treatment on MI/RI. CONCLUSION: This study suggests that depletion of miR-92a promotes upregulation of KLF4 to improve cardiac function, reduce cardiomyocyte apoptosis and further enhance the role of Sevo treatment in alleviating MI/RI.
OBJECTIVE: As some articles have highlighted the role of microRNA-92a (miR-92a) in myocardial ischemia-reperfusion injury (MI/RI), this article aimed to investigate the effect of miR-92a on Sevoflurane (Sevo)-treated MI/RI via regulation of Krüppel-like factor 4 (KLF4). METHODS: An MI/RI rat model was established by ligating the left anterior descending coronary artery. The cardiac function, pathological changes of myocardial tissues, inflammatory response, oxidative stress and cardiomyocyte apoptosis in MI/RI rats were determined. KLF4 and miR-92a expression was detected in the myocardial tissue of rats, and the target relationship between miR-92a and KLF4 was confirmed. RESULTS: Sevo treatment alleviated myocardial damage, inflammatory response, oxidative stress response, and cardiomyocyte apoptosis, and improved cardiac function in MI/RI rats. miR-92a increased and KLF4 decreased in the myocardial tissue of MI/RI rats. KLF4 was targeted by miR-92a. Downregulation of miR-92a or upregulation of KLF4 further enhanced the effect of Sevo treatment on MI/RI. CONCLUSION: This study suggests that depletion of miR-92a promotes upregulation of KLF4 to improve cardiac function, reduce cardiomyocyte apoptosis and further enhance the role of Sevo treatment in alleviating MI/RI.