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目的:探讨胰岛素样生长因子-1(IGR-1)在实验性大鼠肝纤维化过程中的表达状况及白细胞介素-10(IL-10)对肝纤维化大鼠IGF-1表达的影响。方法:建立大鼠肝纤维化模型并行IL-10干预实验。分批从肝纤维化进程中不同阶段的对照组、CCl_4诱导肝纤维化模型组及IL-10干预肝纤维化组的大鼠中取肝脏组织,采用S-P免疫组织化学方法分别检测分析不同组及同组不同阶段大鼠肝组织中IGF-1的表达状况。结果:经CCl_4诱导成功建立大鼠肝纤维化模型。随着肝纤维化程度的进展,IGF-1在肝组织中阳性表达明显增强;经Ridit分析,对照组(38.1％)与肝硬化模型组(92.0％)组间比较IGF-1阳性表达均有显著性差异(P<0.01);IL-10干预肝纤维化组IGF-1阳性表达(71.4％)较肝纤维化模型组均明显减弱,经Ridit分析组间均有显著性差异(P<0.05),且随IL-10干预时间的延长,IGF-1在肝组织中阳性表达均逐渐减弱。结论:IGF-1随着肝纤维化程度的进展阳性表达增强,外源性IL-10可降低CCl_4诱导大鼠肝纤维化中IGF-1的表达。
AIM: To investigate the expression of insulin-like growth factor-1 (IGR-1) in experimental rat liver fibrosis and the effects of interleukin-10 (IL-10) on the expression of IGF-1 in rats with hepatic fibrosis . Methods: The rat model of hepatic fibrosis was established and IL-10 intervention experiment was performed. The rats in different stages of hepatic fibrosis were divided into control group, CCl 4 -induced hepatic fibrosis model group and IL-10 interfered hepatic fibrosis group in batches. The liver tissue was taken from rats in each group. SP immunohistochemical method was used to detect and analyze the different groups IGF-1 expression in rat liver tissue in different stages of the same group. Results: Rat model of hepatic fibrosis was successfully established by CCl_4 induction. With the progression of hepatic fibrosis, the positive expression of IGF-1 in liver tissue was significantly increased. According to Ridit analysis, the positive expression of IGF-1 in control group (38.1%) and cirrhosis model group (92.0% (P <0.01). The positive expression of IGF-1 in IL-10-induced liver fibrosis group (71.4%) was significantly weaker than that in liver fibrosis model group (all P <0.05) ), And with the prolongation of IL-10 intervention, the positive expression of IGF-1 in liver tissue gradually weakened. Conclusion: The positive expression of IGF-1 with the progression of liver fibrosis is enhanced. Exogenous IL-10 can reduce the expression of IGF-1 in CCl 4 -induced liver fibrosis.