大黄酸对糖尿病大鼠肾小管上皮细胞转分化的影响
Effects of rhein on renal tubular epithelial cells transdifferentiation in diabetic rats
目的 观察大黄酸对糖尿病大鼠肾小管上皮细胞-肌成纤维细胞转分化(EMT)的影响.方法 雄性Wistar大鼠随机分为3组:正常对照组(N组,n=12)、糖尿病模型组(D组,n=12)、糖尿病大黄酸干预组[R组,n=12,大黄酸100 mg/(kg·d)灌胃].成模后第8周末及16周末各组分别处死6只大鼠,测定24 h尿蛋白排泄量、血肌酐;HE及MASSON染色法观察肾脏病理改变;免疫组织化学法检测E钙粘蛋白(E-cad)、α平滑肌肌动蛋白(α-SMA)、纤连蛋白(FN)及转化生长因子β1(TGF-β1)的表达.结果 (1)与N组比较,D组大鼠肾小管间质损伤指数、肾间质胶原面积明显增加(P<0.01);(2)D组大鼠肾小管上皮细胞E-cad阳性表达显著低于N组,α-SMA、FN和TGF-β1阳性表达均显著高于N组,E-cad表达和TGF-β1表达呈负相关(rs=-0.60,P<0.05),α-SMA、FN表达和TGF-β1表达呈正相关(rs=0.88,P<0.05;rs=0.91,P<0.01);(3)R组大鼠肾小管间质损伤指数、肾间质胶原面积较D组明显减弱,其肾小管上皮细胞的E-cad的表达较D组明显增加,α-SMA、FN和TGF-β1表达较D组均明显减弱(P<0.01).结论 大黄酸具有减轻糖尿病大鼠肾小管间质病变的肾脏保护作用,其机制可能与下调TGFβ1表达、阻抑EMT有关.
更多Objective To study the effect of rhein on the process of tubular epithelial-mesenchymat transformation in kidney of diabetic rats. Methods Wistar male rats were randomly assigned to 3 groups: Control group (N group, n=12),diabetic group(D group, n=12), rhein treatment group(R group, n=12).The rats of rhein treatment group were treated with daily intragastric administration of periment. The excretion of urinary protein and serum creatine were measured. Histological changes of renal tissue were observed by HE and MASSON stain. Immunohistochemistry was performed to investigate the expression of E-cadherin, α-SMA,FN and TGF-β1 in kidney. Results Compared with the control group, the tubulointerstitial injury and the accumulation of extraeellular matrix protein in diabetic models were obvious(P<0.01).Compared with the control group, the expression of E-cadherin was decreased significantly and the expression of α-SMA,FN and TGF-β1 was increased significantly in diabetic group. E-cadherin was negatively correlated with TGF-β1(rs=-0.60,P<0.05),α-SMA and FN was positively correlated with TGF-β1(rs=0.88,P<0.05;rs:0.91,P<0.01).In comparison with diabetic group,rhein could up-regulate the expression of E-cad and down-regulate the expression of α-SMA and FN in renal tubular epithelial cells(P<0.01).Conclusion Rhein could protect kidney by ameliorating interstitial fibrosis in diabetic rats. The mechanism may be depend on down-regulating the expression of TGF-β1 and suppressing tubular epithelial-mesenchymal transformation.
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