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Therapeutic effect of interleukin-10 on CCl4-induced hepatic fibrosis in rats.

机译:白介素10对CCl4诱导的大鼠肝纤维化的治疗作用。

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AIM: To study the therapeutic effect of exogenous interleukin-10 on CCl4-induced hepatic fibrosis in rats and its possible mechanisms. METHODS: Fourty-seven SD rats were randomly divided into control group (group N) and CCl4-induced hepatic fibrosis model group (group C). After CCl4 was given for 9 wk, the model group was divided into three groups. Rats in group M were put to death immediately,rats in group T were treated with IL-10 for another three wk and then put to death, rats in group R recovered after three weeks and were then killed. The degree of hepatic fibrosis was measured by HE staining and histological activity index (HAI). Histological activity index (HAI), change of collagen types I and III were measured by Picrosirius staining. The expression of TNF-alpha, MMP-2 and TIMP-1 in liver tissue was measured by S-P immunohistochemistry. RESULTS: CCl4- induced experimental rat hepatic fibrosis model was established successfully. The degree of hepatic fibrosis was markedly lower in group T than in groups M and R, and there was no difference between the two groups.The expression of collagen types I and III was significantly suppressed in group T and was slightly suppressed in groups M and R. The positive levels of TNF-alpha, MMP-2 and TIMP-1 in group M increased significantly compared to those in group N (P<0.01). The positive signals decreased significantly in groups T and R (P<0.01),but positive score was significantly lower in group T than in group R (P<0.01). CONCLUSION: Exogenous IL-10 can reverse CCl4-induced hepatic fibrosis in rats. IL-10 may exert its reversible effects on hepatic fibrosis by blocking CCl4-induced inflammation,inhibiting expression of MMP-2 and TIMP-1 and promoting resolution of collagen types I and III.
机译:目的:研究外源白介素10对CCl4诱导的大鼠肝纤维化的治疗作用及其可能的机制。方法:47只SD大鼠随机分为对照组(N组)和CCl4诱导的肝纤维化模型组(C组)。给予CCl4 9周后,将模型组分为三组。 M组大鼠立即处死,T组大鼠再用IL-10治疗3周,然后处死,R组大鼠三周后恢复,然后处死。肝纤维化程度通过HE染色和组织学活性指数(HAI)测量。组织活性指数(HAI),I型和III型胶原蛋白的变化通过Picrosirius染色进行测量。用S-P免疫组织化学法检测肝组织中TNF-α,MMP-2和TIMP-1的表达。结果:成功建立了CCl4诱导的大鼠肝纤维化模型。 T组肝纤维化程度明显低于M和R组,两组间无差异。T组I和III型胶原的表达被明显抑制,M组和M组则被轻度抑制。 R.与N组相比,M组的TNF-α,MMP-2和TIMP-1阳性水平显着增加(P <0.01)。 T和R组的阳性信号明显降低(P <0.01),但T组的阳性评分显着低于R组(P <0.01)。结论:外源IL-10可逆转CCl4诱导的大鼠肝纤维化。 IL-10可能通过阻断CCl4诱导的炎症,抑制MMP-2和TIMP-1的表达并促进I型和III型胶原的分解而对肝纤维化发挥可逆作用。

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