Down-regulation of myocardial infarction associated transcript 1 improves myocardial ischemia-reperfusion injury in aged diabetic rats by inhibition of activation of NF-κB signaling pathway. (25th February 2019)

• Record Type: Journal Article
• Authors: Liu, Yaoxia; Wang, Tao; Zhang, Min; Chen, Ping; Yu, Yerong
• Is Part Of: Chemico-biological interactions. Volume 300(2019)
• Page Start: 111
• Page End: 122
• Publication Date: 2019-02-25
• Subjects: Diabetes -- Myocardial ischemia reperfusion injury -- MIRT1 -- NF-κB signaling pathway -- Myocardial fibrosis -- Oxidative stress; Biochemistry -- Periodicals; Toxicological chemistry -- Periodicals; Biochemistry -- Periodicals; Biologie moléculaire -- Périodiques; Biochimie -- Périodiques; Toxicologie biochimique -- Périodiques; 572
• DOI: 10.1016/j.cbi.2019.01.001
• Languages: English
• ISSNs: 0009-2797

Abstract

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. Highlights: High expression of MIRT1 in myocardial tissue of aged diabetic I/R rats. Diabetes can induce increased cardiac function damage in aged I/R rats. Inhibition of MIRT1 reduces myocardial I/R injury in aged diabetic I/R rats. Inhibition of MIRT1 inhibits NF-κB signaling pathway in aged diabetic I/R rats. MIRT1 regulates myocardial I/R injury in aged diabetic rats by NF-κB pathway.