Yaoxia Liu1, Tao Wang2, Min Zhang3, Ping Chen3, Yerong Yu4. 1. Department of Endocrinology, West China School of Medicine/ West China Hospital, Sichuan University, Chengdu, 610041, PR China; Department of Endocrinology in Elderly, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, 610041, PR China. 2. Department of Pediatric Cardiology, West China Second University Hospital, Sichuan University, Chengdu, 610041, PR China; Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, Chengdu, 610041, PR China; Key Laboratory of Obstetric, Gynecologic and Pediatric Diseases of Sichuan Province, Chengdu, 610041, PR China. 3. Department of Endocrinology in Elderly, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, 610041, PR China. 4. Department of Endocrinology, West China School of Medicine/ West China Hospital, Sichuan University, Chengdu, 610041, PR China. Electronic address: yuyerong0919@163.com.
Abstract
OBJECTIVE: This study is performed to investigate the effect of long chain noncoding RNA myocardial infarction associated transcript 1 (MIRT1) on myocardial ischemia reperfusion (I/R) injury in aged diabetic rats. METHODS: The aged diabetic rat model and myocardial I/R injury model were established. Through injecting MIRT1 siRNA into caudal vein of rats, the cardiac function, myocardial pathological injury, myocardial fibrosis, cardiomyocytes apoptosis, oxidative stress and inflammatory injury of myocardial tissue of rats were measured. RESULTS: For diabetic I/R rats, the expression of MIRT1 in myocardial tissue was increased, the activation of nuclear factor kappa B (NF-κB) signaling pathway was increased, the degree of damage to cardiac function was aggravated, the area of myocardial pathological injury and myocardial fibrosis was enlarged, the degree of cardiomyocytes apoptosis was increased, the degree of oxidative stress and inflammatory injury was increased. After inhibiting the expression of MIRT1, the activation of NF-κB signaling pathway was inhibited, the damage of cardiac function and cardiomyopathy was alleviated, the area of myocardial fibrosis was decreased, the degree of myocardial apoptosis was decreased, the degree of oxidative stress and inflammatory injury was obviously improved. CONCLUSION: Our study highlights that down-regulation of MIRT1 improves myocardial I/R injury in aged diabetic rats by inhibition of activation of NF-κB signaling pathway.
OBJECTIVE: This study is performed to investigate the effect of long chain noncoding RNA myocardial infarction associated transcript 1 (MIRT1) on myocardial ischemia reperfusion (I/R) injury in aged diabeticrats. METHODS: The aged diabeticrat model and myocardial I/R injury model were established. Through injecting MIRT1 siRNA into caudal vein of rats, the cardiac function, myocardial pathological injury, myocardial fibrosis, cardiomyocytes apoptosis, oxidative stress and inflammatory injury of myocardial tissue of rats were measured. RESULTS: For diabetic I/R rats, the expression of MIRT1 in myocardial tissue was increased, the activation of nuclear factor kappa B (NF-κB) signaling pathway was increased, the degree of damage to cardiac function was aggravated, the area of myocardial pathological injury and myocardial fibrosis was enlarged, the degree of cardiomyocytes apoptosis was increased, the degree of oxidative stress and inflammatory injury was increased. After inhibiting the expression of MIRT1, the activation of NF-κB signaling pathway was inhibited, the damage of cardiac function and cardiomyopathy was alleviated, the area of myocardial fibrosis was decreased, the degree of myocardial apoptosis was decreased, the degree of oxidative stress and inflammatory injury was obviously improved. CONCLUSION: Our study highlights that down-regulation of MIRT1 improves myocardial I/R injury in aged diabeticrats by inhibition of activation of NF-κB signaling pathway.