论文部分内容阅读
目的:探讨血管内皮生长因子(VEGF)、诱导型一氧化氮合酶(iNOS)、血管生成素(Angpt)-1及内皮素(ET)-1在大鼠布加综合征(BCS)肝纤维化模型中的表达及意义。方法:结扎雄性SD大鼠肝后段下腔静脉建立BCS动物模型,按数字表法分为对照组(20只)、实验组(80只)和假手术组(80只),实验组及假手术组又各分4个亚组(实验1、3、6、12周,各20只)。各组行免疫组织化学、苏木精-伊红(HE)及马松(Masson)染色,以实时定量聚合酶链反应(Real-time PCR)及蛋白质印迹法(Western blot)检测ET-1、VEGF、iNOS及Angpt-1的表达量。各因子水平在各组间差异采用方差分析,亚组间两两比较采用LSD检验,以皮尔逊(Pearson)及斯皮尔曼(Spearman)法做相关性分析。结果:实验组1、3、6、12周VEGF(1.41±0.18、6.54±0.78、4.19±0.41、2.16±0.25)、iNOS(2.06±0.21、8.88±0.95、4.85±0.51、2.79±0.28)及Angpt-1(9.57±0.91、6.20±1.39、4.53±0.49、2.55±0.33)的mRNA水平均高于对照组(VEGF:0.97±0.08;iNOS:1.01±0.11;Angpt-1:1.01±0.10)及假手术组(VEGF:n F=366.124、412.266;iNOS:n F=443.326、1170.864;Angpt-1:n F=213.868、503.210,n P0.05; Angpt-1:n F=0.969, n P>0.05); the overall difference was statistically significant in the experimental group compared with the control group and the sham group (VEGF:n F=366.124, 412.266; iNOS: n F=443.326, 1170.864; Angpt-1: n F=213.868, 503.210, n P<0.01); the expression of each factor in the subgroups of experimental group was higher than that of control group (VEGF: 0.97±0.08; iNOS: 1.01±0.11; Angpt-1: 1.01±0.10) and sham subgroups at the same time (n P<0.05). The overall differences of mRNA expression of VEGF (1.41±0.18, 6.54±0.78, 4.19±0.41, 2.16±0.25), iNOS (2.06±0.21, 8.88±0.95, 4.85±0.51, 2.79±0.28) and Angpt-1 (9.57±0.91, 6.20±1.39, 4.53±0.49, 2.55±0.33) in the experimental group at each time point after the operation were significant (n F=293.799, 346.260, 137.121, n P<0.01), and the comparison between each subgroup were also statistically significant (n P<0.05). VEGF (1.41±0.18, 6.54±0.78, 4.19±0.41, 2.16±0.25) was positively correlated with iNOS (2.06±0.21, 8.88±0.95, 4.85±0.51, 2.79±0.28) and angpt-1 (9.57±0.91, 6.20±1.39, 4.53±0.49, 2.55±0.33,n r=0.983, 0.364, n P<0.05), and iNOS (2.06±0.21, 8.88±0.95, 4.85±0.51, 2.79±0.28) was positively correlated with angpt-1 (9.57±0.91, 6.20±1.39, 4.53±0.49, 2.55±0.33,n r=0.377, n P<0.05).n Conclusion:The expression of iNOS, Angpt-1 and VEGF in BCS model is increased and positively correlated each other. They are involved in the regulation of intrahepatic and extrahepatic angiogenesis and liver fibrosis in BCS, but the specific mechanism needs further study.