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作 者:顾俊菲[1] 叶山东[1] 汪姗[1] 孙文佳[1] 胡圆圆[1]
机构地区:[1]安徽医科大学附属省立医院内分泌科,安徽合肥230001
出 处:《南京医科大学学报(自然科学版)》2014年第5期607-610,共4页Journal of Nanjing Medical University(Natural Sciences)
基 金:安徽省自然科学基金(11040606M161);安徽高校省级自然科学研究项目(KJ2011A157)
摘 要:目的:观察二甲双胍对大鼠肾小球系膜细胞(mesangial cells,MCs)核因子-κB(nuclear factor-κB,NF-κB)、细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)表达的影响,探讨其肾脏保护机制。方法:体外培养MCs,随机分为正常糖组(NG)、高糖组(HG)及高糖+不同浓度二甲双胍组(M1:0.5 mmol/L;M2:1.0 mmol/L;M3:2.0 mmol/L)。培养48 h后收集各组细胞,采用荧光实时定量聚合酶链式反应法(real time-PCR)检测细胞NF-κB mRNA及ICAM-1 mRNA含量,蛋白质印迹法(Western blot)检测细胞NF-κBp65和ICAM-1蛋白表达水平。结果:①MCs可表达NF-κB、ICAM-1;②与NG组比较,HG组MCs NF-κB、ICAM-1mRNA和蛋白表达增强(P<0.05);③与HG组比较,M3组MCs NF-κB、ICAM-1mRNA相对表达量明显降低,差异有统计学意义(P<0.05);④与HG组比较,M1组、M2组和M3组MCs NF-κBp65、ICAM-1蛋白表达量明显降低,差异有统计学意义(P<0.01)。结论:二甲双胍可抑制肾小球系膜细胞NF-κB、ICAM-1 mRNA和蛋白表达,并具有一定的浓度依赖性,该作用可能是其肾脏保护机制之一。Objective:To observe the effects of metformin on expressions of nuclear factor-κB and intercellular adhesion molecule-1 in cultured rat glomerular mesangial cells(MCs) and explore its reno-protective mechanisms. Methods:MCs were cultured in the medium with normal glucose(group NG), high glucose(group HG),and different concentrations of metformin (group M1, 0.5 mmol/L;group M2, 1.0 mmol/L;group M3, 2.0 mmol/L). After 48h exposure, MCs were collected for mRNA and protein expression of NF-κB, ICAM-1. The expression of NF-κB and ICAM-1 mRNA was analyzed by real time polymerase chain reaction. The expression of NF-κBp65 and ICAM-1 protein was visualized by western blotting . Results:①MCs expressed NF-κB and ICAM-1. ②After stimulated by high glucose, the levels of intracelluar NF-κB, ICAM-1 mRNA and protein expression were significantly increased compared with group NG(P 〈 0.05). ③Compared with group HG, the expression of intracellular NF-κB, ICAM-1 mRNA was significantly decreased in group M3(P 〈 0.05). ④Compared with group HG, the expression of intracellular NF-κBp65 and ICAM-1 protein was significantly decreased in group M1, M2 and M3 in a dose-dependent manner(P 〈 0.01). Conlusion:Metformin can suppress the expression of NF-κB and ICAM-1 in glomerular mesangial cells in a concentration-dependent mode, which may partly contribute to its reno-protection.
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