全反式维甲酸对高糖诱导的HK-2细胞外基质合成的影响及可能机制

发布时间：2018-05-04 08:05

  本文选题：高糖 + 全反式维甲酸　； 参考：《中国老年学杂志》2017年01期

【摘要】：目的探讨全反式维甲酸(ATRA)对高糖诱导HK-2细胞外基质合成的影响及其在延缓糖尿病肾病肾间质纤维化中的可能作用机制。方法将体外培养的HK-2细胞随机分为七组:A组(5.5 mmol/L D-葡萄糖)、B组(30 mmol/L D-葡萄糖)、C组(5.5 mmol/L D-葡萄糖+24.5 mmol/L甘露醇)、D组(10~(-7)mol/L ATRA+30 mmol/L高糖)、E组(10~(-6)mol/L ATRA+30 mmol/L高糖)、F组(10~(-5)mol/L ATRA+30 mmol/L高糖)、G组(10μmol/L Y-27632+30 mmol/L高糖),各组细胞均培养48 h。应用ELISA法检测细胞培养液结缔组织生长因子(CTGF)和Ⅳ型胶原的表达水平;RT-PCR法检测细胞Rho A、ROCK1的表达水平。结果 B组Rho A mRNA及ROCK1 mRNA的表达较A组显著升高(P0.05),D、E、F组Rho A mRNA及ROCK1 mRNA较B组均表达减少(P0.05),且随着ATRA浓度的升高呈现剂量依赖性。G组Rho A mRNA的表达与B组无明显差异,但ROCK1 mRNA的表达较B组显著减少(P0.05);直线相关分析显示高糖组,D、E、F组Rho A mRNA与ROCK1 mRNA表达呈正相关(r=0.854,P=0.030;r=0.895,P=0.016;r=0.883,P=0.020;r=0.867,P=0.025);ELISA结果显示D、E、F组及G组CTGF、Ⅳ型胶原表达较B组显著下降(P0.05),且下降程度与ATRA浓度呈现剂量相关性。结论 ATRA在一定浓度范围内可抑制高糖诱导的HK-2细胞外基质的合成,延缓肾间质纤维化,其机制可能与抑制Rho A/ROCK通路有关。
[Abstract]:Objective to investigate the effect of ATRAA on the synthesis of extracellular matrix of HK-2 induced by high glucose and its possible mechanism in delaying renal interstitial fibrosis of diabetic nephropathy. Methods HK-2 cells cultured in vitro were randomly divided into seven groups: 1: a group (5. 5 mmol/L / L) and 5. 5 mmol/L / D group (n = 30 mmol/L). C group: 5. 5 mmol/L D-glucose 24. 5 mmol/L mannitol group. Group D: 10 mmol/L -7 mol / L ATRA 30 mmol/L high glucose group 10 -6 mol / L ATRA 30 mmol/L high glucose group F group 10 ~ (-5) mol / L ATRA ~ (-30) -5 mol / L / L ATRA 30 mmol/L. In group G, 10 渭 mol/L Y-27632 30 mmol/L high glucose content was observed, and the cells were cultured for 48 h. The expression level of connective tissue growth factor (CTGF) and type 鈪，

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