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干扰素-α对CCl_4诱导的大鼠肝纤维化治疗作用 被引量:6

Curative effect of interferon-α on rat liver fibrosis induced by CCl_4
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摘要 目的:观察干扰素-α对CCl4诱导的SD大鼠肝纤维化治疗作用,并探讨其机制。方法:SD雄性大鼠39只,随机分为正常组(n=10),每只大鼠给予花生油0.003 mL/g皮下注射,共10周。模型组(n=15),每只大鼠给予40%CCl4(CCl4∶花生油=2∶3)0.003 mL/g皮下注射,每周2次,共10周。干扰素-α治疗组(n=14)。每只大鼠给予40%CCl4(CCl4∶花生油=2∶3)0.003 mL/g皮下注射,每周2次,共10周。于第7周皮下注射干扰素α-2b每日10万单位/只,至第10周。于第10周末处死所有大鼠,留取肝组织行HE和Masson染色观察肝脏组织的病理变化及进行肝纤维化分期、半定量评分,采用免疫组织化学检测肝组织中Ⅰ型胶原、α平滑肌激动蛋白(α-smooth muscle actin,α-SMA)、转化生长因子β1(transforming growth factor beta1,TGF-β1)的表达。结果:CCl4诱导的SD大鼠肝纤维化的肝脏病理检查HE染色示,纤维化分期模型组明显高于正常组(P<0.01),干扰素-α治疗组明显低于模型组(P<0.05);Masson染色纤维半定量评分,模型组明显高于正常组(P<0.01),干扰素-α治疗组明显低于模型组(P<0.05)。大鼠肝免疫组织化学染色,I型胶原免疫组化半定量评分模型组明显高于正常组(P<0.01),干扰素-α治疗组明显低于模型组(P<0.05);α-SMA免疫组化半定量评分模型组明显高于正常组(P<0.01),干扰素-α治疗组明显低于模型组(P<0.05);TGF-β1免疫组化表达,模型组明显高于正常组(P<0.01),干扰素-α治疗组明显低于模型组(P<0.05)。结论:干扰素α-2b可降低CCl诱导的SD大鼠肝纤维化,其机制可能与抑制肝星状细胞活化,降低TGF-β1表达有关。 Objective To explore the curative effect and the mechanism of interferon-α (IFN-α) on rat liver fibrosis induced by CCl4. Methods Thirty-nine male SD rats were randomly divided into 3 groups. The rats in the normal control group ( n = 10) received subcutaneous injection of peanut oil (0. 003 mL/g body weight) for 10 weeks. Rat liver fibrosis was induced in 29 rats by 0. 003 mL/g subcutaneous injection of 40% CCl4 ( CCl4: peanut oil = 2:3 ) , twice weekly for 10 weeks. In the 7th week, these 29 rats were randomly divided into a liver fibrosis group without treatment (n = 15) and an IFN-α treatment group (n = 14), which received subcutaneous injection of IFN-α-2b at 10^6 units per rat. The rats' liver tissue was collected and HE and Masson staining were performed to observe of pathological changs, stage of liver fibrosis, and semi-quantitative scoring. Immunohistochemistry was used to detect the expression of Collagen I, α-smooth muscle actin (α-SMA) ,and transforming growth factor- beta 1 (TGF-β1) in the rat liver. Results The stage of liver fibrosis, semi-quantitative scoring of Masson staining, and immunohistochemical staining of Collagen I in the liver fibrosis group were significantly higher than those of the normal controls ( All P 〈 0.01 ) , and those in the IFN-α treatment group were sigificantly lower than those of the liver fibrosis group( P 〈 0.05 ). The semi-quantitative immunohistochemical scoring of α-SMA and TGF-β1 in the liver fibrosis group was significantly higer than those of the normal control ( All P 〈 0. 01 ) , and that in the IFN-α treatment group was signficanthy lower than that of the liver fibrosis group (All P 〈0.05). Conclusion Treatment of IFN-α can decrease the liver fibrogenesis induced by CCl4 in rats. The anti-fibrosis effect of IFN-α may be attributed to the inhibition of the hepatic stellate cells' activation to decrease TGF-β1 expression.
出处 《中南大学学报(医学版)》 CAS CSCD 北大核心 2008年第10期919-925,共7页 Journal of Central South University :Medical Science
基金 湖南省科技厅重大课题(05sk1002-3)~~
关键词 肝纤维化 干扰素-Α I型胶原 α平滑肌激动蛋白 转化生长因子Β1 大鼠 liver fibrosis interferon-α factor β1 Type I collagen rats α-smooth muscle actin transforming growth
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参考文献10

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