贵州医科大学学报

2019, v.44;No.229(10) 1134-1139

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HGF上调SnoN mRNA抑制高糖介导大鼠肾小管上皮细胞纤维病变机制
Study on the Mechanism of HGF Upregulate SnoN mRNA to Inhibit High Glucose Induced Rat Renal Tubular Epithelial Cells Fibrosis

王圆圆;刘慧铭;梁露群;张会芳;向珈谊;郭兵;
WANG Yuanyuan;LIU Huiming;LIANG Luqun;ZHANG Huifang;XIANG Jiayi;GUO Bing;Department of Pathophysiology, School of Basic Medicine, Guizhou Medical University;Guizhou Provincial Key Laboratory of Pathogenesis & Drug Research on Common Chronic Diseases, Guizhou Medical University;

摘要(Abstract):

目的:探讨肝细胞生长因子(HGF)是否通过转录共抑制因子(SnoN)影响高糖介导大鼠肾小管上皮细胞纤维病变。方法:将体外培养NRK-52E细胞分为对照组(NG组,正常糖培养液培养)、高糖对照组(HG组,高糖培养液培养)、10μg/L rhHGF干预组(低剂量rhHGF组, 10μg/L rhHGF高糖培养液培养)及20μg/L rhHGF干预组(高剂量rhHGF组, 20μg/L rhHGF高糖培养液培养);培养48 h时,采用Western blot方法检测各组细胞SnoN、细胞外信号调节激酶1和2(ERK1/2)信号通路及E-钙黏素(E-cadherin)、α-平滑肌肌动蛋白(α-SMA)及胶原蛋白Ⅲ(Col-Ⅲ)蛋白的表达,qRT-PCR技术检测SnoN mRNA的表达。结果:与NG组相较,HG组细胞中α-SMA、Col-Ⅲ蛋白和活化的ERK1/2表达上调(P<0.05),E-cadherin、SnoN蛋白表达下调(P<0.05),SnoN mRNA表达增高(P<0.05);然而与HG组比较,在rhHGF干预组,10μg/L或20μg/L rhHGF均可使NRK-52E细胞α-SMA和Col-Ⅲ蛋白表达减少(P<0.05),而E-cadherin、SnoN蛋白和活化的ERK1/2表达增多(P<0.05),SnoN mRNA表达进一步增高(P<0.05)。结论:HGF阻断或对抗高糖介导肾小管上皮细胞-肌成纤维细胞转分化和间质细胞外基质的沉积,其机制可能是通过活化ERK1/2通路上调SnoN mRNA表达实现。
Objective: To investigate whether hepatocyte growth factor(HGF) affect rat renal tubular epithelial fibrosis through transcriptional co-inhibitor SnoN(Ski-related novel protein N). Methods: NRK-52 E cells were cultured in vitro were divided into control group(NG group, cultivated in normal sugar solution), high sugar group(HG group, cultivated in high sugar solution), 10 μg/L rhHGF intervening group(low dose rhHGF group, cultivated in 10 μg/L rhHGF high dose sugar solution) and 20 μg/L rhHGF intervening group(high dose rhHGF group, cultivated in 20 μg/L rhHGF high dose sugar solution). After cultivated for 48 h, Western blot was used to detect SnoN, extracellular signal-regulated kinase-1 and-2(ERK1/2) signaling pathway, E-cadherin and α-smooth muscle actin(α-SMA) and Collagen III(Col-III) protein expression; qRT-PCR technique was used to detect the expression of SnoN mRNA. Results: Compared with NG group, the expression of α-SMA, Col-Ⅲ and activated ERK1/2 was up-regulated in HG group(P<0.05), while the expression of E-cadherin and SnoN protein was down-regulated(P<0.05); the expression of SnoN mRNA was increased(P<0.05). However, compared with HG group, in rhHGF group, 10 μg/L or 20 μg/L rhHGF could lower the expression of α-SMA and Col-Ⅲ protein(P<0 05), while the expression of E-cadherin, SnoN and activated ERK1/2 increased(P<0.05); SnoN mRNA expression was further improved(P<0.05). Conclusion: HGF blocks or antagonizes the process of epithelial-mesenchymal transition(EMT) and the deposition of interstitial extracellular matrix(ECM) in renal tubular epithelial cells mediated by high glucose by activating ERK1/2 pathway to up-regulate the expression of SnoNmRNA.

关键词(KeyWords): 糖尿病肾病;肝细胞生长因子;转录共抑制因子;细胞外信号调节激酶;肾小管上皮细胞;上皮细胞-肌成纤维细胞转分化
diabetic nephropathy;hepatocyte growth factor;transcriptional co-inhibitor;extracellular signal regulated kinase;renal tubular epithelial cells;epithelial-mesenchymal transition

Abstract:

Keywords:

基金项目(Foundation): 国家自然科学基金(81760131);; 贵州省科技厅科技支撑计划[黔科合支撑(2017)2837];; 贵州省学术新苗项目[黔科合平台人才(2017)5718]

作者(Author): 王圆圆;刘慧铭;梁露群;张会芳;向珈谊;郭兵;
WANG Yuanyuan;LIU Huiming;LIANG Luqun;ZHANG Huifang;XIANG Jiayi;GUO Bing;Department of Pathophysiology, School of Basic Medicine, Guizhou Medical University;Guizhou Provincial Key Laboratory of Pathogenesis & Drug Research on Common Chronic Diseases, Guizhou Medical University;

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DOI: 10.19367/j.cnki.1000-2707.2019.10.004

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