摘要
AIM： To study the therapeutic effect of exogenous interleuldn-10 on CCl4-induced hepatic fibrosis in rats and its passible 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 H 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-α, HHP-2 and TIMP-1 in liver tissue was measured by S-P immunohis tochemistry.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 H 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 H and R. The positive levels of TNF-α, HHP-2 and TIHP-1 in group H 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）. CONCLUS10N： 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 HHP-2 and TIMP-1 and promoting resolution of collagen types Ⅰ and Ⅲ.
瞄准：在老鼠和它的可能的机制在导致 CCl4 的肝的纤维变性上学习外长的 interleukin-10 的治疗学的效果。方法：四十 -- 七只 SD 老鼠随机被划分成控制组(组 N ) 和导致 CCl4 的肝的纤维变性模型组(组 C ) 。在 CCl4 为 9 wk 被给以后，模型组被划分成三个组。在组 M 的老鼠立即被放到死亡，在组 T 的老鼠为另一三 wk 与 IL-10 被对待然后放了到死亡，在组 R 的老鼠在三个星期以后恢复了并且然后被打死。肝的纤维变性的度被测量由他染色并且组织学的活动索引(HAI ) 。组织学的活动索引(HAI ) ，骨胶原类型的变化我和 III 被染色的 Picrosirius 测量。在肝织物的 TNF-alpha， MMP-2 和 TIMP-1 的表示被 S-P 免疫组织化学测量。结果：CCl4- 导致了试验性的老鼠肝的纤维变性模型成功地被建立。肝的纤维变性的度比在组 M 和 R 在组 T 是显著地更低的，并且二个组之间没有差别。骨胶原类型的表示我和 III 显著地在组 T 被镇压并且稍微在组 M 和 R 被压制。在组 M 的 TNF-alpha， MMP-2 和 TIMP-1 的积极层次在组 N (P<0.01 ) 与那些相比显著地增加了。积极信号在组 T 和 R (P<0.01 ) 显著地减少了，但是积极分数比在组 R (P<0.01 ) 在组 T 是显著地更低的。结论：外长的 IL-10 能在老鼠颠倒导致 CCl4 的肝的纤维变性。IL-10 可以由堵住导致 CCl4 的发炎在肝的纤维变性上施加它的可逆效果，禁止 MMP-2 和 TIMP-1 的表示并且支持骨胶原类型的分辨率我和 III。
基金
Supported by Nature Science Foundation of Fujian Province. No.2005D094 and No.C0410025
