The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Shandong University Qilu Hospital, Jinan 250012, Shandong, China.
Department of Cardiology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu, China.
Biomed Pharmacother. 2016 Jul;81:258-264. doi: 10.1016/j.biopha.2016.04.020. Epub 2016 Apr 21.
Curcumin has properties of anti-inflammation, anti-oxidation, anti-infection and anti-tumor, benefiting for the treatment of many diseases. The present study was aimed to investigate the role of curcumin in myocardial infarction (MI) and its potential mechanism involving transcription factor specific protein 1 (SP1).
After receiving curcumin, C57BL/6 mice subjected to left anterior descending (LAD) coronary artery occlusion to induce MI model. Infarct size was measured by triphenyl tetrazolium chloride staining. In vitro experiments, mouse cardiac myocytes (MCM) subjected to hypoxia after the incubation of curcumin, miR-7a/b and SP1 expression levels were detected by real-time PCR and western blot. Caspase-3 activity and TUNEL assay were performed to assess the cell apoptosis.
In animal experiments, curcumin significantly reduced the infarct size compared with the control. It also up-regulated miR-7a/b expression and down-regulated SP1 expression. In hypoxia-induced MCM, curcumin led to the decrease of cell apoptosis. Transfected MCM with miR-7a/b inhibitor, curcumin induced the decrease of cell apoptosis and SP1 expression was reversed. Transfected with pcDNA-SP1, the decrease of cardiac myocytes apoptosis after the treatment of curcumin was also reversed.
Curcumin pre-treatment protected against hypoxia-induced cardiac myocytes apoptosis through the up-regulation of miR-7a/b and the down-regulation of SP1 expression.
姜黄素具有抗炎、抗氧化、抗感染和抗肿瘤的特性,有利于治疗多种疾病。本研究旨在探讨姜黄素在心肌梗死(MI)中的作用及其涉及转录因子特异性蛋白 1(SP1)的潜在机制。
给予姜黄素后,C57BL/6 小鼠接受左前降支(LAD)冠状动脉闭塞以诱导 MI 模型。通过三苯基四氮唑氯化物染色测量梗死面积。在体外实验中,姜黄素孵育后,小鼠心肌细胞(MCM)处于缺氧状态,通过实时 PCR 和 Western blot 检测 miR-7a/b 和 SP1 的表达水平。通过 caspase-3 活性和 TUNEL 测定评估细胞凋亡。
在动物实验中,与对照组相比,姜黄素显著减少了梗死面积。它还上调了 miR-7a/b 的表达并下调了 SP1 的表达。在缺氧诱导的 MCM 中,姜黄素导致细胞凋亡减少。转染 miR-7a/b 抑制剂的 MCM 后,姜黄素诱导的细胞凋亡减少,SP1 表达被逆转。转染 pcDNA-SP1 后,姜黄素处理后心肌细胞凋亡的减少也被逆转。
姜黄素预处理通过上调 miR-7a/b 和下调 SP1 表达来防止缺氧诱导的心肌细胞凋亡。