Ischemic postconditioning attenuates the inflammatory response in ischemia/reperfusion myocardium by upregulating miR‑499 and inhibiting TLR2 activation
Autor: | Xin‑Yue Zhang, Guo-Qiang Zhong, Jian-Jun Meng, Qing-Jie Li, Zheng Huang, Rong‑Hui Tu, Dong-Xiao Wang |
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Rok vydání: | 2020 |
Předmět: |
Male
0301 basic medicine Cancer Research medicine.medical_treatment Ischemia Down-Regulation Myocardial Reperfusion Injury Inflammation Pharmacology Biochemistry Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine Genetics medicine Animals microRNA-499 ischemic postconditioning Receptor Molecular Biology Protein kinase C Cardioprotection Chemistry Myocardium Interleukin Articles medicine.disease Toll-Like Receptor 2 Up-Regulation MicroRNAs 030104 developmental biology Cytokine Oncology inflammation Apoptosis 030220 oncology & carcinogenesis Molecular Medicine medicine.symptom protein kinase C |
Zdroj: | Molecular Medicine Reports |
ISSN: | 1791-3004 1791-2997 |
DOI: | 10.3892/mmr.2020.11104 |
Popis: | Toll-like receptor 2 (TLR2)-mediated myocardial inflammation serves an important role in promoting myocardial ischemic/reperfusion (I/R) injury. Previous studies have shown that miR-499 is critical for cardioprotection after ischemic postconditioning (IPostC). Therefore, the present study evaluated the protective effect of IPostC on the myocardium by inhibiting TLR2, and also assessed the involvement of microRNA (miR)-499. Rat hearts were subjected to 30 min of ischemia and 2 h of reperfusion. The IPostC was 3 cycles of 30 sec of reperfusion and 30 sec of re-occlusion prior to reperfusion. In total, 90 rats were randomly divided into six groups (n=15 per group): Sham; I/R; IPostC; miR-499 negative control adeno-associated virus (AAV) vectors + IPostC; miR-499 inhibitor AAV vectors + IPostC; and miR-499 mimic AAV vectors + IPostC. It was identified that IPostC significantly decreased the I/R-induced cardiomyocyte apoptotic index (29.4±2.03% in IPostC vs. 42.64±2.27% in I/R; P |
Databáze: | OpenAIRE |
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