Shenqiwan Ameliorates Renal Fibrosis in Rats by Inhibiting TGF-β1/Smads Signaling Pathway.
Shenqiwan Ameliorates Renal Fibrosis in Rats by Inhibiting TGF-β1/Smads Signaling Pathway.
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参芪丸通过抑制TGF-β1/Smads信号通路改善大鼠肾纤维化
DOI：
10.1155/2017/7187038
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发表时间：
2017
期刊：
影响因子：
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通讯作者：
Li C
中科院分区：
文献类型：
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作者：
Chen H;Xu Y;Yang Y;Zhou X;Dai S;Li C
上皮-间充质转化（epithelial -mesenchymal transition， EMT）是指上皮细胞向间充质细胞的转化。越来越多的证据表明，EMT是肾间质纤维化（RIF）的一个关键点。中药参芪丸被广泛应用于临床治疗慢性肾脏疾病，但其作用机制尚不清楚。本研究的目的是探讨SQW对肾纤维化的影响及其与TGF-β1/Smads信号通路的关系。建立腺嘌呤（150 mg/kg）大鼠模型，分别以1.5 g/kg、3 g/kg、6 g/kg不同浓度的SQW灌胃。对照组和模型组均给予等量生理盐水。阳性对照组给予依那普利（4 mg/kg）治疗。给药后第21天处死动物。结果表明，SQW能显著减轻腺嘌呤引起的肾脏病理损伤，增加E-cadherin基因和蛋白表达，降低肾样品中Vimentin的表达。此外，SQW通过上调Smad7有效抑制p-Smad2/3的mRNA和蛋白表达。这些结果表明，SQW可能通过抑制TGF-β1/Smads信号通路来减缓肾纤维化的进展。
Epithelial-mesenchymal transition (EMT) refers to the transition of epithelial cells into mesenchymal cells. Emerging evidence suggests that EMT is a key point in renal interstitial fibrosis (RIF). Traditional Chinese Medicine Shenqiwan (SQW) is widely used in clinical treatment of chronic kidney disease, but the underlying mechanism remains unclear. The purpose of this study is to investigate the effect of SQW on renal fibrosis and its association with TGF-β1/Smads signaling pathway. A rat model of adenine (150 mg/kg) was established and intragastrically treated with various concentrations of SQW at dose of 1.5 g/kg, 3 g/kg, and 6 g/kg. Control group and model group were given the same volume of saline. Meanwhile, the positive control group was treated with Enalapril (4 mg/kg). Animals were sacrificed on 21st day after administration. The results showed that SQW could significantly relieve renal pathological damage caused by adenine, increase gene and protein expression of E-cadherin, and decrease the expression of Vimentin in kidney samples. In addition, SQW efficiently inhibited the mRNA and protein expression of p-Smad2/3 by upregulating Smad7. These results suggest that SQW could slow down the progression of renal fibrosis, possibly by inhibiting TGF-β1/Smads signaling pathway.