摘要
目的探讨结缔组织生长因子(connective tissue growth factor,CTGF)是否具有抑制人增生性瘢痕成纤维细胞(hypertrophic scar fibroblast,HSF)凋亡的作用及磷脂酰肌醇3激酶/蛋白激酶B信号通路(PI3K/PKB)是否介导该效应。方法体外培养HSF,实验分3组:空白对照组,②CTGF刺激组(10ng/ml),③PI3K抑制剂LY294002(10μmol/L)预处理后CTGF刺激组(LY294002组)。应用免疫印迹技术检测30min后蛋白激酶B的活化情况,应用流式细胞术检测细胞凋亡。结果和空白对照组相比,CTGF组细胞凋亡指数下降,蛋白激酶B的活化水平升高,具有统计学差异(P<0.05);LY294002组细胞凋亡指数上升,蛋白激酶B的活化水平没有升高,与CTGF组比较具有显著性差异(P<0.05)。结论CTGF能够抑制HSF凋亡,PI3K/PKB介导该效应。
Objective To explore whether the anti-apoptotic human hypertrophic scar fibroblasts is mediated by phosphatidylinosi effect of connective tissue growth factor on tol 3-kinase/protein kinase B （PI3K/PKB） signal pathway. Methods The cultured human hypertrophic scar fibroblasts were divided into three groups： control group, connective tissue hibitor LY294002 （ 10 μmol/L） growth factor （ 10 ng/ml） stimulated group, the group pretreated with PI3K inand stimulated with connective tissue growth factor. Levels of phosphorylated PKB were examined by Western blotting in human hypertrophic scar fibroblasts that were stimulated with con- nective tissue growth factor for 30 min. Flow cytometry was used to detect the apoptosis ratio of the cells. Resuits Compared with the control group, the apoptosis ratio of the connective tissue growth factor stimulated group decreased （ P 〈 0. 05 ） and the activation of PKB increased （ P 〈 0. 05 ）. However, the apoptosis ratio of connective tissue （P 〈0.05）, and tire tissue growth naling pathway. growth factor stimulated group after the pretreatment of PI3K inhibitor LY294002 increased the activation of PKB remained as the control group. Conclusion It is proven that eonneetire tissue growth factor can inhibit the apoptosis of human hypertrophic scar fibroblasts through PI3K/PKB signaling pathway.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2008年第10期921-923,共3页
Journal of Third Military Medical University
基金
国家自然科学基金(30400472)~~
