摘要
目的探讨 CCL4 诱导的肝纤维化模型鼠肝组织 Smad2/3,Smad7,TIMP-1,TGF-β1 的表达及氯沙坦干预后对其表达的影响。方法 Wistar大鼠 40 只,随机分成正常对照组、模型组、氯沙坦预防组和治疗组,采用 CCL4 皮下注射构建肝纤维化模型。行 HE 和 VG 染色,判断肝组织炎症和纤维化的程度。免疫组化方法检测各组 Smad2,3 Smad7 和 TIMP-1,TGF-β1 的表达。结果氯沙坦预防组和治疗组的肝组织炎症和纤维化程度明显低于模型组;Sm ad2,3 TIM P-1 TG F-β1 在氯沙坦预防组和治疗组的阳性表达均低于模型组( 分别为 Smad2,3:1.69 ±0.42,1.90 ±0.59,2.51 ±0.39;TIM P-1:1.09 ±0.28,1.32 ±0.23,2.60 ±0.35;TGF-β1:1.65±0.31,2.04±0.42,2.72±0.36),P <0.05;Sm ad7 在氯沙坦预防组和治疗组的阳性表达高于模型组( 分别为2.50±0.35,2.21±0.59,0.47±0.26),P <0.05。Smad2,3 Smad7 TIM P-1 和 TGF-β1 在氯沙坦预防组和治疗组的表达差异无显著性,P >0.05。结论氯沙坦抗肝纤维化作用可能与抑制 TGF-β1,TIMP-1,Smad2,3 和促进Smad7 的表达有关。
[Objective] To study the expression of Smad2/3, Smad7, TIMP-1 and TGF-β1 in hepatic fibrosis induced by the exposure of CCL4 and the effects of Losartan on them. [Methods] A total of 40 healthy Wistar rats were divided into four groups randomly： control group, model group, prevention group and treatment group. Hepatic fibrosis models were established in latter 3 groups by injection CCL4. Liver tissue sections were stained with Hematoxylin-eosin and van Gieson to evaluate the degree of inflammation and hepatic fibrosis. The expression of Smad2/ 3, Smad7, TIMP-1 and TGF-β1 were measured by immunohistochemical staining in liver tissue. [Results] The degree of inflammation and hepatic fibrosis in model group was higher than that in control group, prevention group and treatment group. The expression of Smad2/3, TIMP-I and TGF-β1 in model group was stronger than that in prevention group and treatment group （Smad2/3： 2.60±0.35, 1.09±0.28, 1.32±0.23; TIMP-1： 2.51±0.39, 1.69±0.42, 1.90± 0.59; TGF-β1： 2.72±0.36, 1.65±0.31, 2.04±0.42; respectively）, P 〈0.05. The expression of Smad7 in model group was weaker than that in prevention group and treatment group （0.47±0.26, 2.50±0.35, 2.21±0.59, respectively）, P 〈 0.05. There were no differences on the expression of them between prevention group and treatment group, P 〉0.05. [Conclusion] Losartsn may play a important role in attenuating the progression of rat hepatic fibrosis by inhibiting expression of Smad2,3 TIMP-1, TGF-β1 and promoting expression of Smad7.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2007年第4期385-388,共4页
China Journal of Modern Medicine
