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黄芪当归合剂抑制马兜铃酸I诱导的肾小管上皮细胞损伤

[Astragalus and angelica mixture inhibits the renal tubular epithelial cell injury induced by aristolochic-acid I].

作者信息

Li Biao, Tang Jia-wei, Cai Shao-qing, Li Xiao-mei

机构信息

Department of Nephrology, Peking University First Hospital, Beijing 100034, China.

出版信息

Beijing Da Xue Xue Bao Yi Xue Ban. 2006 Aug 18;38(4):381-4.

PMID:16892142
Abstract

OBJECTIVE

To investigate whether Chinese herb astragalus and angelica mixture (A&A) have influence on the renal tubular epithelial cell injury induced by aristolochic-acid I.

METHODS

Human proximal tubular epithelial cell line HK-2 was pre-treated with AA-I (2.5 mg/L) for 4 hours. Cells were then treated with or without A&A for additional 44 hours. Cell apoptosis was evaluated by using FACS. Secreted fibronectin (FN) and TGF-beta1 levels were assayed by ELISA. The changes of AA-I-induced FN, TGF-beta1 level and the rate of apoptosis were compared before and after A&A treatment.

RESULTS

There was basement secretion of TGF-beta1 by HK-2 cells (7.05+/-1.98 microg/L). Both normal serum (N-S) and A&A could not induce the cells to secret TGF-beta1(6.35+/-1.99 microg/L and 6.57+/-2.19 microg/L, vs. control, P>0.05). AA-I could induce the TGF-beta1 secretion by HK-2 cells (18.26+/-5.98 microg/L, vs. control, P<0.05). A&A could block AA-I-induced TGF-beta1 secretion by 63.5% (6.66+/-0.70 microg/L, vs. AA-I, P<0.05). It also suppressed AA-I-induced cell apoptosis by 93.7% (3.32%+/-0.41% vs. 19.19%+/-6.32% respectively, P<0.001) and FN secretion by 44% (1.64+/-1.11 folds vs. 2.93+/-0.87 folds respectively, P<0.05).

CONCLUSION

A&A inhibits AA-I induced injury in human renal proximal tubule epithelial cells, whose mechanism may be partially through blocking TGF-beta1 secretion.

摘要

目的

研究中药黄芪当归合剂(A&A)对马兜铃酸I诱导的肾小管上皮细胞损伤是否有影响。

方法

人近端肾小管上皮细胞系HK-2先用马兜铃酸I(2.5mg/L)预处理4小时。然后细胞再用或不用A&A处理44小时。采用流式细胞术评估细胞凋亡。用酶联免疫吸附测定法检测分泌型纤连蛋白(FN)和转化生长因子-β1(TGF-β1)水平。比较A&A处理前后马兜铃酸I诱导的FN、TGF-β1水平及凋亡率的变化。

结果

HK-2细胞有基础水平的TGF-β1分泌(7.05±1.98μg/L)。正常血清(N-S)和A&A均不能诱导细胞分泌TGF-β1(分别为6.35±1.99μg/L和6.57±2.19μg/L,与对照组相比,P>0.05)。马兜铃酸I能诱导HK-2细胞分泌TGF-β1(18.26±5.98μg/L,与对照组相比,P<0.05)。A&A能使马兜铃酸I诱导的TGF-β1分泌减少63.5%(6.66±0.70μg/L,与马兜铃酸I组相比,P<0.05)。它还使马兜铃酸I诱导的细胞凋亡减少93.7%(分别为3.32%±0.41%和19.19%±6.32%,P<0.001),使FN分泌减少44%(分别为1.64±1.11倍和2.93±0.87倍,P<0.05)。

结论

A&A抑制马兜铃酸I诱导的人肾近端小管上皮细胞损伤,其机制可能部分是通过阻断TGF-β1分泌实现的。

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