论文部分内容阅读
目的观察扶肾降浊方对大鼠系膜增生性肾炎的治疗作用,探讨扶肾降浊方对系膜增生性肾炎大鼠肾组织TGF-β1、CTGF及Ang-Ⅱ表达的影响。方法将正常Wister大鼠40只随机分为对照组、模型组、苯那普利组(西药组)、扶肾降浊方组(中药组)。模型组与药物干预组分别制备慢性系膜增生性肾炎模型,16周后留尿检测24h尿蛋白,取血测定血尿素氮(BUN)、血肌酐(Scr);处死大鼠并留取肾组织,HE及Masson染色观察肾脏病理形态学改变,免疫荧光方法检测各组肾组织中TGF-β1、CTGF、Ang-Ⅱ的表达。结果与对照组大鼠相比,模型组24h尿蛋白定量、BUN、Scr明显升高,肾间质TGF-β1、CTGF、Ang-Ⅱ阳性表达明显(P<0.05),并出现细胞浸润及纤维化、肾小管萎缩。两给药物组各指标均呈弱阳性表达。两给药组的表达量较模型组明显下降,免疫荧光指标比较P<0.05。结论扶肾降浊方可抑制大鼠Ms PGN模型肾组织TGF-β1、CTGF、Ang-Ⅱ的表达,减弱肾间质细胞与基质的增生,延缓肾纤维化的进程。
Objective To observe the therapeutic effect of Fufang Jiangzhuo Fang on rat mesangial proliferative glomerulonephritis and to explore the effect of Fu Shen Jiang Zhuo Fang on the expression of TGF-β1, CTGF and Ang-Ⅱ in rat mesangial proliferative glomerulonephritis rats. Methods Forty normal Wister rats were randomly divided into control group, model group, benazepril group (western medicine group) and Fu Shen Jiang Zhuo Fang group (traditional Chinese medicine group). The model group and the drug intervention group were respectively prepared chronic mesangial proliferative glomerulonephritis model. After 16 weeks, urine samples were collected to detect urinary protein for 24h. Blood samples were taken for determination of blood urea nitrogen (BUN) and serum creatinine (Scr) The pathological changes of kidney were observed by HE and Masson staining. The expression of TGF-β1, CTGF and Ang-Ⅱ in each group were detected by immunofluorescence. Results Compared with the control group, 24 h urinary protein, BUN and Scr in model group were significantly increased (P <0.05), while the expression of TGF-β1, CTGF and Ang-Ⅱ in renal interstitium was significantly increased Atrophy of tubules. The two groups of drug indicators were weakly positive expression. Compared with the model group, the expression levels of the two administration groups were significantly decreased, the immunofluorescence index was P <0.05. Conclusion Fufang Jiangzhuo Fang can inhibit the expression of TGF-β1, CTGF and Ang-Ⅱ in renal tissue of rats with Ms PGN, weaken the proliferation of renal interstitial cells and matrix, and delay the process of renal fibrosis.