论文部分内容阅读
目的 研究 β胡萝卜素对四氯化碳 (CCl4 )诱导的实验性大鼠肝纤维化的影响 ,并探讨其作用机制。方法 ①在CCl4 诱导实验性大鼠肝纤维化 3周后 ,同时给予 β胡萝卜素 2 5 0 0 0 0U/kg体重 ,每周 2次灌胃 ,同时设正常及CCl4 对照组。②观察肝脏组织学及超微结构改变 ,检测大鼠肝组织羟脯氨酸含量 (生化法 )、α2 Ⅰ型胶原RNA(点杂交法 )和转化生长因子β1(TGFβ1,免疫组化法 )的表达。结果 β胡萝卜素防治组中 ,肝纤维化程度计分显著低于CCl4 组 (P <0 .0 5 ) ,肝星形细胞中的脂滴数量少于正常对照组 ,但多于CCl4 对照组 ;β胡萝卜素防治组中 ,肝组织羟脯氨酸含量显著低于CCl4 组 (P <0 .0 5 ) ;肝脏α2 (Ⅰ )型前胶原RNA和TGFβ1表达显著低于CCl4 组 (P <0 .0 5 )。结论 上述剂量的 β胡萝卜素 ,能显著降低由CCl4 诱导的大鼠肝纤维化的程度 ,其作用机制可能与抑制TGFβ1在肝组织中的表达和减少肝脏星形细胞中视黄醇脂滴的丢失有关
Objective To study the effect of β-carotene on carbon tetrachloride (CCl4) -induced hepatic fibrosis in rats and its mechanism of action. Methods ① After 3 weeks of CCl4-induced hepatic fibrosis in rats, β-carotene was given at the same time as 25 000 000 U / kg body weight twice a week. Normal and CCl4 control groups were also established. ② The histological and ultrastructural changes of the liver were observed. The content of hydroxyproline (biochemical method), α2 type collagen (dot blot hybridization) and TGFβ1 (immunohistochemistry) expression. Results The scores of hepatic fibrosis in β-carotene control group were significantly lower than those in CCl4 group (P <0.05). The number of lipid droplets in hepatic stellate cells was less than that of normal control group, but more than that of CCl4 control group. The content of hydroxyproline in liver tissue in β-carotene control group was significantly lower than that in CCl4 group (P <0.05). The expression of α2 (Ⅰ) procollagen and TGFβ1 in liver tissue was significantly lower than that in CCl4 group (P <0. 0 5). Conclusion The above-mentioned dose of β-carotene can significantly reduce the degree of hepatic fibrosis induced by CCl4 in rats, and its mechanism may be related to inhibiting the expression of TGFβ1 in liver tissue and reducing the loss of retinol lipid droplets in liver astrocytes