4.7 Article

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

Journal

CHEMICO-BIOLOGICAL INTERACTIONS
Volume 300, Issue -, Pages 111-122

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.cbi.2019.01.001

Keywords

Diabetes; Myocardial ischemia reperfusion injury; MIRT1; NF-kappa B signaling pathway; Myocardial fibrosis; Oxidative stress

Funding

  1. National Natural Science Foundation of China [81701888]
  2. Health and Family Planning Commission Foundation of Sichuan Province [17PJ262]

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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-kappa B) 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-kappa B 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-kappa B signaling pathway.

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