黄芪对肾间质纤维化大鼠肾组织Snail的影响及机制

目的 探讨黄芪对环孢素A诱导的肾病大鼠肾组织炎症反应及Snail的影响.方法 采用环孢素A制模,大鼠分为对照组、模型组和实验组.采用Masson染色观察肾间质改变,ELISA法检测TNF-α含量,免疫组化检测Snail 蛋白的表达及分布,RT-PCR检测Snail mRNA的表达水平.结果 (1)Masson染色:模型...

Effects of astragalus mongholicus on expression of snail in rats with cyclosporin A-induced nephropathy

AIM To explore the effect of astragalus mongholicus(AM) on inflammation and the expression of snail in rats with cyclosporin A induced nephropathy. Methods Rats were induced chronic kidney disease by gavage with CsA. Rats were randomly divided into three groups：control group、CsA group and AM group group．Renal interstitial fibrosis was graded according to Masson staining. The inflammatory factor TNF- was tested in ELISA. The expression of Snail1 was examined by immunohistochemistry and RT-PCR. Results 1. Masson staining: There are little green collagen deposition in the control group，and there are a large number of green interstitial collagen deposition in CsA group. However, The collagen fibers of renal interstitial in AM group reduce significantly than the CSA group (P <0.05). 2. ELISA results : The content of TNF-α was the highest in CSA group. Compared with CSA group, the content of TNF-α were significantly lower in AM group(P<0.05). 3. The expression of snail: ①Immunohistochemical results: The Snail expression of control group was the least. The Snail expression in CSA group was increased significantly compared with the control group,which was mainly in the nucleus of tubular epithelial cells, glomerular visceral epithelial cells . The Snail expression in AM group were significantly lower than CSA group (P<0.05);② RT-PCR results: Compared with the Control group, the Snail mRNA levels in test groups were significantly increased (P <0.05). Compared with CSA group, the Snail mRNA levels of AM group were significantly lower (P <0.05). Conclusion Astragalus mongholicus attenuates renal fibrosis in in rats with cyclosporin A induced nephropathy. It decreased the expression of snail directly, which may be related to the inhibition of inflammation.