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目的：为探讨星形细胞中过度表达的胰岛素样生长因子Ⅰ(IGF-Ⅰ)对肝细胞损害的保护作用。方法：分别选取肝星形细胞(HSC)中转基因IGF-Ⅰ过度表达的转基因小鼠(TG)，并以转基因IGF-Ⅰ在HSC中无表达的同窝野生型小鼠(WT)对照组，用四氯化碳诱导小鼠急性肝损害模型，以玉米油灌胃作安慰剂对照；并检测以下指标：血浆ALT、AST水平测定，四氯化碳灌胃前后测定体重，肝脏病理组织学检查。结果：在四氯化碳诱导小鼠急性肝损害模型中，WT组血浆AST水平明显高于WT正常对照组(P<0.0001)，而TG组无显著差异(P=0.25)；TG和WT组的血浆ALT均增高，但TG组升高程度较少；而且TG组的体重明显高于WT组(P<0.01)；进一步观察病理片，TG组仅有小面积的肝细胞坏死，炎症局限于肝小叶的中央区，肝小叶仍保持完整，损害较WT组轻。结论：小鼠的肝星形细胞中IGF-Ⅰ过度表达对四化碳诱导小鼠急性肝损害有保护作用。
Objective: To investigate the protective effect of overexpressed insulin-like growth factor Ⅰ (IGF-Ⅰ) on hepatocyte damage in astrocytes. Methods: TG transgenic mice with overexpression of IGF-Ⅰ in HSC were selected and treated with transgenic IGF-Ⅰ in wild-type WT mice without HSC. Acute liver injury model was induced by carbon tetrachloride (CCl4) and corn oil was given as placebo control. The following indexes were measured: plasma ALT and AST levels, body weight before and after carbon tetrachloride (GCC) administration, liver histopathology . Results: In carbon tetrachloride-induced acute liver injury model, the level of plasma AST in WT group was significantly higher than that in WT control group (P <0.0001), but not in TG group (P = 0.25) (P <0.01). Further observation of pathological sections showed that only a small area of liver cells were necrotic in TG group, and the inflammation was limited to Liver lobular central area, hepatic lobules remain intact, damage than the WT group lighter. CONCLUSION: Overexpression of IGF-I in hepatic stellate cells of mice has a protective effect on acute liver injury induced by carbon tetrachloride in mice.