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目的探讨线粒体三磷酸腺苷(ATP)敏感性钾通道(mitoK ATP)在槲皮素抑制乳大鼠心肌细胞肥大中的作用。方法利用体外培养模型,以苯肾上腺素(PE)10μmol/L诱导心肌细胞肥大,在mitoK ATP通道阻断剂5-羟基癸酸(5-HD)存在情况下,槲皮素设25、50、100μmol/L 3个剂量;用Lowry法检测心肌细胞蛋白质含量,消化分离法及计算机图像分析系统检测心肌细胞体积,逆转录-聚合酶链反应(RT-PCR)法检测心肌细胞心房钠尿肽(ANP)的mRNA表达,Western印迹法测定K ATP通道K ir6.2亚基表达。结果与对照组比较,模型组大鼠心肌细胞总蛋白质含量[(27.45±2.45)μg]增加,细胞体积[(2 278±156)μm3]增大,ANP的mRNA表达增多,K ir6.2表达无明显变化;与模型组比较,槲皮素50、100μmol/L组心肌细胞蛋白含量[分别为(21.15±1.39)、(19.28±2.23)μg]减少、细胞体积[分别为(1 656±230)、(1 398±298)μm3]减小,K ir6.2表达增加,呈剂量依赖性。而在加入5-HD后,槲皮素对PE诱导心肌肥大的抑制作用消失。结论槲皮素可通过开放mitoK ATP通道抑制PE诱导的乳大鼠心肌细胞肥大。
Objective To investigate the role of mitoK ATP in the inhibition of cardiomyocyte hypertrophy induced by quercetin in neonatal rats. Methods Myocardial cell hypertrophy was induced by phenylephrine (PE) 10 μmol / L in vitro. In the presence of 5-hydroxydecanoate (5-HD), a mitoK ATP channel blocker, 100μmol / L 3 doses. Cardiac myocyte protein content was detected by Lowry’s method. Cardiomyocyte volume was detected by digestion and computerized image analysis system. Atrial natriuretic peptide (atrial natriuretic peptide) was detected by reverse transcription-polymerase chain reaction (RT-PCR) ANP) mRNA expression was measured by Western blot K K ATP channel K ir6.2 subunit expression. Results Compared with the control group, the total protein content of myocardial cells in model group increased ([(27.45 ± 2.45) μg] and the cell volume [(2 278 ± 156) μm3] increased, the mRNA expression of ANP increased, K ir6.2 expression Compared with the model group, the protein content of cardiomyocytes in quercetin 50,100μmol / L group was (21.15 ± 1.39) and (19.28 ± 2.23) μg, respectively, while the cell volume [(1 656 ± 230 ), (1 398 ± 298) μm3], K ir6.2 expression increased in a dose-dependent manner. However, the inhibitory effect of quercetin on PE-induced cardiac hypertrophy disappeared after adding 5-HD. Conclusion Quercetin inhibits cardiomyocyte hypertrophy induced by PE in isolated rat by opening mitoK ATP channel.