高级检索

    大黄素对高糖诱导的大鼠肾小球系膜细胞TGF-β1/ERK1/2及FN蛋白表达的影响

    Effects of emodin on TGF-β1/ERK1/2 and FN protein expression in rat glomerular mesangial cells induced by high glucose

    • 摘要: 目的探讨大黄素(emodin,EMO)对高糖诱导的大鼠肾小球系膜细胞(glomerular mesangial cells,MCs)转化生长因子-β1(TGF-β1)/细胞外信号调节激酶1/2(ERK1/2)及细胞外基质(extracellular matrix,ECM)FN蛋白表达的影响。方法将常规培养的MCs分为正常组(NG,5.56 mmol/L葡萄糖)、 甘露醇组(MA,5.56 mmol/L葡萄糖+24.44 mmol/L甘露醇)、溶剂组(0.1% DMSO+30 mmol/L葡萄糖)、高糖组(HG,30 mmol/L葡萄糖)及大黄素干预组(1 μmol/L、10 μmol/L EMO+30 mmol/L葡萄糖)。CCK-8检测细胞增殖情况;Western blotting检测各组细胞TGF-β1、p-ERK1/2、FN蛋白表达。结果与正常组比较,高糖培养48 h MCs增殖显著(P<0.05,P<0.01),p-ERK1/2、TGF-β1、FN蛋白表达明显增高(P<0.05);与高糖组比较,大黄素干预组能抑制MCs增殖,并显著降低p-ERK1/2、TGF-β1、FN蛋白表达(P<0.05或P<0.01)。结论大黄素能抑制高糖诱导下的MCs细胞增殖,下调TGF-β1、p-ERK1/2、FN蛋白表达,从而发挥对糖尿病肾病(diabetic nephropathy,DN)的防治作用。

       

      Abstract: Objective To investigate the effects of emodin (EMO) on the TGF-β1/ERK1/2, extracellular matrix (ECM) and FN protein in rat glomerular mesangial cells (MCs) induced by high glucose. MethodsMCs were divided into four groups: a normal control group (NG, 5.56 mmol/L glucose), a mannitol group (MA, 5.56 mmol/L+24.44 mmol/L mannitol), a solvent group (0.1%DMSO+30 mmol/L glucose), a high glucose group (HG, 30 mmol/L glucose) and an Emodin intervention group (1 μmol/L, 10 μmol/L EMO+30 mmol/L glucose). The cell proliferation was measured by CCK-8 assay. The levels of TGF-β1, p-ERK1/2 and FN were detected by Western blotting. ResultsCompared with the NG group, the HG group presented obvious proliferation after cultivation for 48 h (P<0.05 or P<0.01) and produced significantly increased levels of p-ERK1/2, TGF-β1 and FN (P<0.05). Compared with the HG group, the Emodin intervention group showed suppressed proliferation and remarkably reduced levels of p-ERK1/2, TGF-β1, and FN (P<0.05 or P<0.01). ConclusionsEmodin can inhibit the proliferation of MCs induced by high glucose and down-regulate the levels of p-ERK1/2, TGF-β1 and FN, which plays a role in the prevention and treatment of diabetic nephropathy.

       

    /

    返回文章
    返回