论文部分内容阅读
目的构建缺陷型TGFβ1Ⅱ型受体的表达质粒,观察其对人工免疫性大鼠肝纤维化的影响。方法运用基因重组技术,构建大鼠缺陷型TGFβ1Ⅱ型受体表达质粒载体,将其导入CCl4诱导肝纤维化的大鼠体内,观察其对大鼠肝纤维化的影响。结果经酶切和DNA测序鉴定缺陷型TGFβ1Ⅱ型受体真核表达质粒载体构建成功,经缺陷型TGFβ1Ⅱ型受体表达质粒处理的大鼠肝纤维化程度轻,血清中PCⅢ、Ⅳ-C、HA和LN均较未经处理组低。结论经缺陷型TGFβ1Ⅱ型受休表达质粒处理后可减轻CCl导致的肝纤维化增生。
Objective To construct the expression plasmid of defective TGFβ1 Ⅱ receptor and observe its effect on hepatic fibrosis in artificial immune rats. Methods The recombinant TGFβ1 receptor expression plasmid vector was constructed by gene recombination technique and then introduced into CCl4-induced hepatic fibrosis in rats to observe its effect on hepatic fibrosis in rats. Results The recombinant eukaryotic expression plasmids of TGFβ1 Ⅱ receptor were identified successfully by restriction enzyme digestion and DNA sequencing. The hepatic fibrosis of rats treated with defective TGFβ1 receptor expression plasmid was light, and the levels of PCⅢ, Ⅳ-C, HA And LN were lower than the untreated group. Conclusion Defective TGFβ1 type Ⅱ retired expression plasmids can reduce the hepatic fibrosis induced by CCl.