中文摘要：

目的观察黄芪注射液对转化生长因子β1（TGF-β1）诱导的体外培养的人肾小管上皮细胞（HK-2）转分化（EMT）过程的影响,揭示黄芪注射液治疗肾间质纤维化（RIF）的具体作用机制。方法以正常培养的HK-2细胞为正常组,TGF-β1（8×10-9mg/L）刺激48 h为模型组,TGF-β1（8×10-9mg/L）与黄芪注射液（8×10-6mg/L）共培养48 h为治疗组。倒置相差显微镜下观察细胞形态变化,免疫组化染色法观察细胞内E-钙依赖黏附素（E-cadherin）和a-平滑肌肌动蛋白（a-SMA）的表达变化。结果倒置相差显微镜下观察发现模型组细胞形态经历了由上皮细胞样转变为成纤维细胞样的改变,而治疗组中成纤维细胞数目较模型组减少,并可见大量的上皮样细胞;免疫组化显示模型组细胞中a-SMA的表达较正常组增多,E-cadherin的表达减少,而治疗组细胞中E-cadher-in的表达较模型组增多,a-SMA的表达降低。结论黄芪注射液可在一定程度上抑制由TGF-β1诱导的体外培养HK-2细胞的表型改变,减少细胞内a-SMA的表达,增加E-cadherin的表达,阻断或逆转其EMT的进程。

英文摘要：

Objective To observe the influence of Huangqi Injection on the epithelial-myofibroblast transdifferentiation （EMT） induced by transforming growth factor β1 （TGF-β1） in human renal tubular epithelial cells （HK-2） cultured in vitro, and reveal the detail effective mechanism in the treatment of renal interstitial fibrosis （RIF）. Methods HK-2 cells were divided into 3 groups, and in normal group HK-2 ceils were normally cultured, in model group, stimulated with TGF-β1 （8 ×10 -9 mg/L） for 48 hours, and in treatment group, cultured （8×10-6 rag/L） for 48 hours. The together with TGF-β1 morphologic changes （8 × 10 -9 mg/L） and Huangqi Injection of HK-2 were observed with the inverted phase contrast microscope, and expressions of E-cadherin and a-smooth muscle actin （a-SMA） were observed by using immunohistochemistry assay. Results The observation results of the inverted phase contrast microscope showed that the morphologic changes experienced from epithelial-like transform to fibroblast-like transform in model group, and fibroblasts decreased and a lot of epithelioid cells were observed in treatment group. The results of immunohistochemistry assay showed that the expression of a-SMA increased and expression of E-cadherin decreased in model group compared with normal group, while in treatment group, expression of E-cadherin increased and expression of a-SMA decreased compared with model group. Conclusion Huangqi Injection can inhibit to a certain extent the phenotypic alternation induced by TGF-β1 in HK-2 cells, reduce the expression of a-SMA, improve the expression of E-cadherin, and block or reverse EMT progress.