论文部分内容阅读
目的 观察携带人非分泌型尿激酶型纤溶酶原激活物cDNA的复制缺陷型腺病毒pAd-△uPA对大鼠肝纤维化的影响。方法 运用DNA重组技术,构建携带人非分泌型尿激酶型纤溶酶原激活物cDNA的复制缺陷型腺病毒pAd-△uPA,通过门静脉注射将其导入大鼠肝纤维化模型体内;通过逆转录一聚合酶链反应(RT-PCR),Ⅰ、Ⅲ型胶原的免疫组织化学以及Von Gieson胶原染色法观察腺病毒pAd-△uPA对大鼠肝纤维化的影响。结果pAd-△uPA可在大鼠肝脏中表达,其表达产物可促进肝脏中Ⅰ、Ⅲ型胶原的降解(P<0.05),但对病理形态学的影响尚不显著(P>0.05)。结论腺病毒pAd-△uPA可促进肝纤维化肝脏中Ⅰ、Ⅲ型胶原的降解。
Objective To observe the effect of replication-defective adenovirus pAd-△ uPA carrying human non-secreted urokinase-type plasminogen activator cDNA on hepatic fibrosis in rats. Methods Recombinant adenovirus pAd-△ uPA carrying human non-secreted urokinase-type plasminogen activator cDNA was constructed by DNA recombination technique and then introduced into rat hepatic fibrosis model by portal vein injection. Polymerase chain reaction (RT-PCR), immunohistochemistry of collagen types I and III and Von Gieson collagen staining were used to observe the effect of adenovirus pAd-uPA on hepatic fibrosis in rats. Results The expression of pAd- △ uPA in the liver of rats was observed. The expression of pAd- △ uPA could promote the degradation of collagen type Ⅰ and Ⅲ in the liver (P <0.05), but the pathological changes were not significant (P> 0.05). Conclusion Adenovirus pAd-Δ uPA can promote the degradation of type Ⅰ and type Ⅲ collagen in hepatic fibrosis.