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目的研究 CCl_4诱导鼠肝血管生成因子表达与肝纤维化(LF)及肝硬变(LC)病变的关系.方法 SD 雄性6mo 龄鼠50只,随机分成2组,40只用于造模,10只为对照.实验鼠以3mL·kg~(-1)皮下多点注射500mL·L~(-1)CCl_4(用液状石蜡配制),2次·wk~(-1)对照组不处理.分别于实验2,5,8及12wk 解剖造模鼠10只,作冰冻、石蜡切片及VEGF,α-SMA 及ⅧR Ag 免疫组化观察.结果实验2 wk 鼠体质量略下降而肝质量增加,5 wk 始肝质量下降,至8 wk～12 wk 最明显(P<0.01),且肝表面伴结节形成,组织学证实已发生 LC.免疫组化显示,在实验2 wk VEGF 阳性肝细胞局限于病变周围,部分肝窦内皮细胞α-SMA,ⅧR Ag示阳性表达,以后随肝血管病变加重而上述因子表达强度及分布范围渐增加,提示两者关系密切.结论肝细胞在 LF 及 LC 发展中担当一重要角色.
Objective To investigate the relationship between hepatic fibrosis (LF) and cirrhosis (LC) induced by CCl_4 in rats.Methods Fifty male SD rats of 6 months old were randomly divided into 2 groups, 40 for modeling, 10 Only for the control mice were injected subcutaneously with 3mL · kg -1 subcutaneously 500mL·L -1 CCl 4 (formulated with liquid paraffin), 2 times · wk -1 control group were not treated. 10 rats were dissected at 2, 5, 8 and 12 weeks after operation to observe the expression of VEGF, α-SMA and Ⅷ R Ag in frozen and paraffin sections.Results In 2 wk mice, the quality of rats decreased slightly while the liver mass increased 5 The quality of the liver at the beginning of wk decreased to the highest level at 8 wk ~ 12 wk (P <0.01), and the formation of nodules on the liver surface was confirmed by histology. Immunohistochemistry showed that in the experimental 2 wk VEGF positive hepatocytes were confined to The expression of α-SMA and Ⅷ R Ag in some sinusoidal endothelial cells around the lesion was positive, and then with the increase of hepatic vascular disease, the expression intensity and distribution range of the above-mentioned factors gradually increased, suggesting the close relationship between them.Conclusion The development of hepatocytes in the development of LF and LC Play an important role.