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目的:探讨生地黄和熟地黄对单侧输尿管梗阻模型(UUO)大鼠肾间质纤维化的作用及其机制。方法:雄性SD大鼠随机分为生地黄水煎液组、熟地黄水煎液组、模型对照组、假手术组,每组5只。生地黄水煎液组、熟地黄水煎液组分别按生地黄、熟地黄剂量1.6 g/(kg·d)灌胃给药14 d,测定血清肌酐(Scr)、尿素氮(BUN)。HE染色、Masson染色观察肾脏组织病理学变化,免疫印迹检测TGF-β1、α-SMA和Collagen-Ⅰ的表达。结果:与模型组比较,各给药组大鼠Scr、BUN值显著降低(P<0.05);肾小球玻璃样病变减轻,肾小管囊性扩张和空泡变性程度缓解,胶原沉积减少,肾间质纤维化程度明显改善;TGF-β1、α-SMA和Collagen-Ⅰ表达显著降低(P<0.05)。与熟地黄水煎液组比较,生地黄水煎液组的Scr、BUN值较低,胶原沉积较少,肾间质纤维化改善较明显,α-SMA表达显著减少(P<0.05)。结论:生地黄和熟地黄均能缓解肾间质纤维化,以生地黄作用较强,其作用机制可能与下调TGF-β1、α-SMA和Collagen-Ⅰ的表达有关。
Objective: To investigate the effect of Radix Rehmanniae and Rehmanniae Radix on renal interstitial fibrosis in rats with unilateral ureteral obstruction (UUO) and its mechanism. Methods: Male Sprague-Dawley rats were randomly divided into five groups, namely: Radix Rehmanniae Preparata, Radix Rehmanniae Preparata, model control group and sham operation group. Radix Rehmanniae Decoction and Radix Rehmannia Preparata Decoction groups were respectively given intragastrically for 14 days by radix rehmanniae and Radix Rehmanniae Preparata at a dose of 1.6 g / (kg · d) for determination of serum creatinine (Scr) and blood urea nitrogen (BUN). The pathological changes of kidney were observed by HE staining and Masson staining. The expressions of TGF-β1, α-SMA and Collagen-Ⅰ were detected by Western blotting. Results: Compared with the model group, the Scr and BUN values of rats in each group were significantly decreased (P <0.05), the glomerular lesion of glomeruli lessened, the degree of cystic dilatation and vacuolar degeneration of glomeruli were relieved, collagen deposition was reduced, The degree of interstitial fibrosis significantly improved; the expressions of TGF-β1, α-SMA and Collagen-Ⅰ were significantly decreased (P <0.05). Compared with the group, the Scr and BUN values of the SD group were lower, collagen deposition was less, renal interstitial fibrosis improved significantly, α-SMA expression was significantly reduced (P <0.05). CONCLUSION: Rehmannia glutinosa and Rehmannia glutinosa can relieve renal interstitial fibrosis with strong rehmannia. Its mechanism may be related to down-regulating the expression of TGF-β1, α-SMA and Collagen-Ⅰ.