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目的探讨肾病I号方醋酸乙酯提取物(ethyl acetate extract of Shenbingyihao Decoction,EASD)对肾纤维化大鼠转化生长因子-β1(TGF-β1)、α-平滑肌肌动蛋白(α-SMA)表达的影响。方法 50只SD大鼠随机分为假手术组、模型组、洛丁新(洛丁新片1.67 mg/kg)组、肾病I号方(生药18.75 g/kg)组、EASD(EASD,300 mg/kg)组,除假手术组外,其他各组采用单侧输尿管结扎的方法制备单侧输尿管梗阻(UUO)大鼠模型。各组ig给药14 d后处死大鼠,采集血清,检测尿素氮(BUN)和血肌酐(Scr)水平,取肾组织行HE和Masson染色评价肾小管间质纤维化损伤程度,采用免疫组织化学染色方法和实时荧光定量PCR(RT-PCR)法检测TGF-β1、a-SMA蛋白及m RNA的表达情况。结果与假手术组比较,模型组和3个给药组大鼠血清Scr、BUN升高(P<0.05),间质纤维化程度加重(P<0.05),肾组织TGF-β1、a-SMA表达明显增多(P<0.05)。与模型组比较,3个给药组大鼠的血清Scr、BUN下降(P<0.05),肾组织TGF-β1、a-SMA表达下降(P<0.05)。结论肾病I号方及EASD能够延缓肾纤维化的发生发展,其作用机制可能是通过下调TGF-β1、a-SMA的表达,从而达到保护肾脏的作用。
Objective To investigate the effect of ethyl acetate extract (EASD) on the expression of transforming growth factor-β1 (TGF-β1) and α-smooth muscle actin (α-SMA) Impact. Methods Fifty Sprague-Dawley rats were randomly divided into three groups: sham-operated group, model group, Lotensin (1.67 mg / kg), Nephropathy I (18.75 g / kg), EASD (300 mg / kg) .Unilateral sham operation was performed in all the groups except the sham operation group. Unilateral ureteral obstruction (UUO) rat model was established. Rats in each group were sacrificed 14 days after the administration, serum was collected, the levels of BUN and Scr were measured, and the extent of renal tubulointerstitial fibrosis was evaluated by HE and Masson staining. Immunohistochemistry The expression of TGF-β1, a-SMA protein and m RNA were detected by chemical staining and real-time fluorescence quantitative PCR (RT-PCR). Results Compared with the sham operation group, the levels of Scr and BUN in the model group and the three administration groups were significantly increased (P <0.05), the degree of interstitial fibrosis was increased (P <0.05), the expression of TGF-β1, The expression was significantly increased (P <0.05). Compared with the model group, the serum levels of Scr and BUN decreased (P <0.05) and the expressions of TGF-β1 and a-SMA in the three groups decreased (P <0.05). Conclusion Nephropathy I and EASD can delay the development of renal fibrosis, and its mechanism may be through the down-regulation of TGF-β1, a-SMA expression, so as to protect the kidneys.