Jia Lili, Wang Liang, Liu Wenxue, Qian Guanglei, Jiang Xiufang, Zhang Zhimian
Qilu Hospital of Shandong University, Jinan, Shandong 250012, P.R. China.
Department of Nephrology, Qilu Hospital of Shandong University, Jinan, Shandong 250012, P.R. China.
Exp Ther Med. 2018 Aug;16(2):1350-1354. doi: 10.3892/etm.2018.6297. Epub 2018 Jun 13.
The present study intended to investigate the effect of fluvastatin on cardiomyocyte apoptosis after myocardial infarction in rats. Eighty myocardial infarction rat models were established and randomly divided into 4 groups (n=20): experimental group (n=20) was given fluvastatin treatment; sham operation group (n=20) and normal control group (n=20) were given saline. The dose of fluvastatin was 20 mg/(kg·d), and irrigation gavage was given for 1 week. Western blot analysis and reverse transcription-quantitative PCR (RT-qPCR) were used to detect the expression of TLR4 mRNA and protein in cardiomyocytes. TUNEL method was used to detect the apoptosis of cardiomyocytes. After fluvastatin treatment for 1 week, RT-qPCR found that compared with myocardial infarction group, the TLR4 mRNA expression of fluvastatin treatment group and normal control group was significantly increased, and the differences between groups were a statistically significant difference (P<0.05). Western blot analysis showed that compared with the myocardial infarction group, the expression of TLR4 protein in normal control group, sham operation group and fluvastatin treatment group were significantly decreased, and they all were statistically significant (P<0.05). TUNEL method found that compared with the myocardial infarction group, the fluvastatin treatment group could significantly reduce the apoptosis of cardiomyocytes (19.2±3.8%), and the difference was statistically significant (P<0.05). Fluvastatin can inhibit myocardial infarction and decrease cardiomyocyte apoptosis by increasing the expression of TLR4-like receptor.
本研究旨在探讨氟伐他汀对大鼠心肌梗死后心肌细胞凋亡的影响。建立80只心肌梗死大鼠模型，随机分为4组（n = 20）：实验组（n = 20）给予氟伐他汀治疗；假手术组（n = 20）和正常对照组（n = 20）给予生理盐水。氟伐他汀剂量为20 mg/(kg·d)，灌胃给药1周。采用蛋白质免疫印迹法（Western blot）和逆转录定量聚合酶链反应（RT-qPCR）检测心肌细胞中TLR4 mRNA和蛋白的表达。采用TUNEL法检测心肌细胞凋亡情况。氟伐他汀治疗1周后，RT-qPCR检测发现，与心肌梗死组比较，氟伐他汀治疗组和正常对照组TLR4 mRNA表达显著升高，组间差异有统计学意义（P<0.05）。Western blot分析显示，与心肌梗死组比较，正常对照组、假手术组和氟伐他汀治疗组TLR4蛋白表达均显著降低，差异均有统计学意义（P<0.05）。TUNEL法检测发现，与心肌梗死组比较，氟伐他汀治疗组可显著减少心肌细胞凋亡（19.2±3.8%），差异有统计学意义（P<0.05）。氟伐他汀可通过增加TLR4样受体表达抑制心肌梗死并减少心肌细胞凋亡。
