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腺病毒包装的胰岛素样生长因子结合蛋白相关蛋白1对大鼠肝组织中NF-κB p65表达的影响及意义

发布时间:2018-03-17 20:36

  本文选题:肝硬化 切入点:胰岛素样生长因子结合蛋白质 出处:《中华消化病与影像杂志(电子版)》2014年04期  论文类型:期刊论文


【摘要】:目的探讨腺病毒包装的胰岛素样生长因子结合蛋白相关蛋白1(Ad-IGFBPrP1)对大鼠肝组织中NF-κB p65的表达影响及意义。方法 32只健康雄性SD大鼠随机分为4组,每组8只。正常对照组:尾静脉注射生理盐水;阴性对照Ad-EGFP组:尾静脉注射腺病毒包装的增强型绿色荧光蛋白(Ad-EGFP);Ad-IGFBPrP1 2周组:尾静脉注射Ad-IGFBPrP1;Ad-IGFBPrP1 4周组:尾静脉注射Ad-IGFBPrP1。分别于注射2周、4周末乙醚麻醉大鼠,取肝左叶固定、包埋、切片。行HE染色,观察肝组织病理改变;苦味酸-天狼星红染色观察肝组织中胶原纤维含量的变化;免疫组织化学染色观察IGFBPrP1、核因子κBp65(NF-κBp65)、α-平滑肌肌动蛋白(α-SMA)、纤维连接蛋白(Fn)的表达及分布。结果 HE和苦味酸-天狼星红染色显示:与正常对照组、阴性对照Ad-EGFP组的正常肝组织相比,Ad-IGFBPrP1组肝组织出现病理改变且发生纤维化(P0.01)。免疫组织化学染色显示:Ad-IGFBPrP1组肝组织中IGFBPrP1、NF-κB p65、α-SMA、Fn的表达较正常对照组、阴性对照Ad-EGFP组明显增强(P0.01);Ad-IGFBPrP1 4周组的表达高于2周组(P0.01)。结论 Ad-IGFBPrP1经尾静脉注射成功转染进入大鼠,引起肝组织中NF-κB p65表达增高,最终导致肝组织纤维化,提示IGFBPrP1致肝纤维化的机制之一可能通过NF-κB信号转导通路实现。
[Abstract]:Objective to investigate the effect and significance of adenovirus-packaged insulin-like growth factor binding protein-associated protein (1Ad-IGFBPrP1) on the expression of NF- 魏 B p65 in rat liver. Methods 32 healthy male SD rats were randomly divided into 4 groups. 8 rats in each group. Normal control group: normal saline was injected into tail vein; Ad-EGFP group: Ad-EGFBPrP1 group: Ad-IGFBPrP1 group: Ad-IGFBPrP1 group: Ad-IGFBPrP1 group: Ad-IGFBPrP1 group: Ad-IGFBPrP1 group: Ad-IGFBPrP1 group: Ad-IGFBPrP1 group: Ad-IGFBPrP1 group. The pathological changes of liver tissue were observed by HE staining and the changes of collagen fibers in liver tissue were observed by picric acid-Sirius red staining. Immunohistochemical staining was used to observe the expression and distribution of IGFBPrP1, NF- 魏 Bp65, NF- 魏 Bp65, 伪 -smooth muscle actin (伪 -SMAN). Results HE and picric acid-Sirius red staining showed that the expression and distribution of 伪 -smooth muscle actin (伪 -SMAN) were similar to those of normal controls. Compared with Ad-IGFBPrP1 group, the normal liver tissue of the negative control group showed pathological changes and fibrosis P0.01.The immunohistochemical staining showed that the expression of IGFBPrP1- 魏 B p65 and 伪 -SMAFN in the liver tissue of the control group was higher than that of the normal control group. The expression of P0.01- IGFBPrP1 in the negative control Ad-EGFP group was significantly higher than that in the 2-week group. Conclusion the expression of NF- 魏 B p65 in liver tissue was increased and the liver fibrosis was induced by successful transfection of Ad-IGFBPrP1 through tail vein into rats. The results suggest that one of the mechanisms of hepatic fibrosis induced by IGFBPrP1 may be achieved by NF- 魏 B signal transduction pathway.
【作者单位】: 山西医科大学第一医院消化科;山西医科大学第一医院科研实验中心;
【基金】:山西省回国留学人员重点科研资助项目(2012-重点4) 太原市科技明星项目(120247-04)
【分类号】:R575

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