KGF-1二硫键突变体对肝纤维化的保护作用  

The Preliminary Study of KGF-1 Disulfide Bond Mutants Defense Mechanism to Hepatic Fibrosis

作　　者：谢敏[1,2] 万颖 张增涛 何建军 杨黎 范开[1,2] 

机构地区：[1]重庆理工大学药学与生物工程学院,重庆400054 [2]重庆富进生物医药有限公司,重庆400041

出　　处：《重庆理工大学学报（自然科学）》2012年第4期45-49,共5页Journal of Chongqing University of Technology：Natural Science

基　　金：国家科技重大专项资助项目(2012zx09103301-052);重庆市自然科学基金资助项目(CSTC2007BB5412)

摘　　要：观察KGF-1二硫键突变体对人肝星状细胞的抑制作用和其对试验性肝损伤的修复作用,同时探讨二硫键对蛋白质生物活性的影响。运用CCl4诱导的肝纤维化模型对△23KGF-1组、△23Ser102 KGF-1组(不含二硫键)和△23Ser102 C40-C106 KGF-1组(含二硫键)进行体内抗纤维化活性的比较,并研究其对人肝星状细胞系的抑制作用。结果表明,与模型组相比,KGF-1突变体的各项指标均优于模型组,并且△23Ser102 KGF-1可明显抑制人肝星状细胞系的生长,可见KGF-1突变体不含二硫键组对大鼠试验性肝损伤有明显保护作用。此外实验还证明二硫键的有无会直接影响蛋白质的生物活性。The study observed the inhibition and anti-fibrosis effect of KGF-1 mutant protein on rats hepatic fibrosis induced by CCl4 model, and discussed the relationship of its disulfide bond and func- tion. The SD rats CCl4 model with liver fibrosis were utilized to evaluate the bioactivities of KGF-1 deleted 23 amino acids, KGF-1 mutant with no disulfide bond and KGF-1 mutant with Cys40-Cysl02 disulfide bond. HSC would be used to evaluate the bioactivities of them. Compared with the model group, the biochemical indicator of controlled group was much better. KGF-1 mutant with no disulfide bond has the obvious effect on experimental liver damage, which proved that disulfide bond could affect the bioactivity of protein directly.

关 键 词：重组人角质细胞生长因子-1突变体 二硫键 肝纤维化 四氯化碳 

分 类 号：Q78[生物学—分子生物学]