泽泻醇B抑制C3a介导的人肾小管上皮细胞间充质转分化的实验研究

目的 探讨泽泻醇B能否抑制C3a介导的肾小管上皮细胞间充质转分化(epithelial-mesenchymal transition，EMT)。方法 将体外培养的人肾小管上皮细胞(HK-2)分别用5 ng/mL转化生长因子β(transforming growth factor-β，TGF-β)、0.1 μmol C3a和0.1 μmol C3a加10 μmol泽泻醇B进行干预。分别采用RT-PCR、Western blot和细胞免疫荧光法检测HK-2细胞C3、α-平滑肌肌动蛋白（α-SMA）和上皮钙黏蛋白（E-cadherin） mRNA及蛋白表达。结果 经C3a刺激后，HK-2细胞C3 mRNA和蛋白表达明显增加(P<0.01)，α-SMA mRNA及蛋白表达明显增加(P<0.01)，E-cadherin mRNA及蛋白表达明显减少(P<0.01)。与经外源性C3a干预组比较，经泽泻醇B干预后，HK-2细胞α-SMA mRNA及蛋白表达明显减少(P<0.01)，E-cadherin mRNA及蛋白表达明显增加(P<0.05)。结论 外源性C3a能诱导肾小管上皮细胞发生EMT，泽泻醇B可抑制C3a诱导的EMT。

Alisol B Inhibited Complement 3a-induced Human Renal Tubular Epithelial to Mesenchymal Transition

Objective To study whether alisol B could inhibit complement 3a (C3a) induced renal tubular epithelial-mesenchymal transition (EMT). Methods The in vitro cultured human renal tubular epithelial HK-2 cells were intervened with 5 ng/mL transforming growth factor-β (TGF-β), 0.1 μmol C3a, and 0.1 μmol C3a+10 μmol alisol B, respectively. The mRNA and protein expressions of α-SMA, E-cadherin, and C3 were detected using RT-PCR, Western blot, and immunofluorescence, respectively. Results The mRNA and protein expressions of C3 in HK-2 cells were up-regulated after intervention of C3a (P<0.01), the mRNA and protein expressions of α-SMA in HK-2 cells were obviously enhanced (P<0.01), the mRNA and protein expressions of E-cadherin obviously decreased (P<0.01). When compared with the group intervened by exogenous C3a, after intervention of alisol B, the mRNA and protein expressions of α-SMA in HK-2 cells were obviously reduced (P<0.01), the mRNA and protein expressions of E-cadherin obviously increased (P<0.05). Conclusions Exogenous C3a could induce renal tubular EMT. Alisol B was capable of suppressing C3a induced EMT.