目的:探讨三七总皂苷对阿霉素肾病大鼠肾组织转化生长因子-β1(transforming growth factor-β1,TGF-β1)表达的影响。方法:将45只Wistar雄性大鼠,适应性喂养1周,测尿蛋白阴性后,随机分为正常组、假手术组、模型组、苯那普利组、三七总皂苷组,每组9只。每周测大鼠体重,每2周收集大鼠24h尿量,测24h尿蛋白定量;10周后处死大鼠,分离血清检测BUN、Scr、Cho、TG、TP和AIb,应用HE、Masson染色,观察肾组织病理学改变,免疫组化方法观察三七总皂苷对阿霉素肾病大鼠肾组织TGF—Bl表达的影响。结果:三七总皂苷能够减轻阿霉素肾病大鼠肾组织病理损害,增加阿霉素肾病大鼠体重,减少尿蛋白排泄、提高血TP和Alb水平,降低BUN和scr水平改善。肾功能;正常组及假手术组肾脏固有细胞胞浆中有较少的TGF-pl表达;三七总皂苷组TGF-pl的表达与模型组相比显著减少(P〈0.05)。结论:三七总皂苷能减轻阿霉素肾病大鼠的肾脏病理损害、降低BUN、Scr、调节TG、TP和Alb水平,对阿霉素肾病大鼠肾功能有一定的保护作用,其机制可能是通过降低阿霉素肾病大鼠肾组织TGF-p1的表达而发挥作用。
Objective:To investigate the effects of Panaxnotoginseng on expression of transforming growth factor-β1 (TGF-β1 )in adriamycin nephropathy rats. Methods: 45 male wistar rats were checked to be urinary protein excretion negative and then randomly divided into 5 groups: normal group, model group, sham operation group, Benazepril treatment group, Panaxnotoginseng treatment groups. Renal tissues were examined by light microscopy at the 10th week after operation. HE staining,masson were applied to explore histological and pathological changes in the renal interstitium. Changes in 24 - hour urinary protein excretion, renal function, serum BUN, serum creatinine, Cho, TP, and Alb were also examined. Immunohistochemistry was used to measure the expression of TGF -β1 in the nephridial tissue. Results: Compared with the model group rats, proteinuria, BUN, serum creatinine Cho, TP, Alb in rats treated with Panaxnotoginseng were significantly reduced. Glomerulosclerosis change in Panaxnotoginseng group was also significantly ameliorated. Panaxnotoginseng could significantly decrease the expression of TGF-β1, and there was no significant difference between Panaxnotoginseng treatment group and model group( P 〈 0.05). Conclusion: Panaxnotoginseng could decrease 24 - hour urinary protein,serum BUN,serum creatinine,Cho and hoisted TP, Alb. It is a potential agent in preventing and treating adriamycin - induced nephrosis. Panaxnotoginseng may suppress the development of fibrosis, at least in part via down - regulating the expression of TGF-β1.