目的:探讨CTGF刺激人增生性瘢痕成纤维细胞STATs蛋白活化的情况。方法:原代培养人增生性瘢痕成纤维细胞,将其分为:①对照组:人增生性瘢痕成纤维细胞纽;②增生性瘢痕成纤维细胞外源性重组CTGF刺激组。取0min、5min、10min、20min、30min、45min、60min、90min八个相点,时分别采用MTT检测细胞增殖,western-blot检测各组之间a-平滑肌肌动蛋白(a-smoothmuscle actin,a-SMA)的变化趋势以及各时相点STATl、STAT2、STAT3、STAT4、STAT5、STAT6蛋白活化(磷酸化)情况。结果:在确定成纤维细胞增殖以及a-SMA表达变化趋势以②-①组顺序递减的前提下(P〈0.05),用western—blot观测两组STATs蛋白活化情况,发现:STATl蛋白磷酸化水平以②-①组顺序递减(P〈0.01);STAT2-6均有不同程度的磷酸化,但不以②-①组顺序递减。结论:STAT1可能在CTGF促进人增生性瘢痕成纤维细胞增殖和分化过程中可能发挥着重要作用,以上研究结果为抑制瘢痕纤维化及挛缩提供了新的研究方向。
Objective To investigate the activation of STATs in CTGF-induced proliferation and differentiation of human hypertrophic scar fibroblast (hHSFB). Methods To cultivate hHSFB with primary cultivation,then to divide the cells into two groups: ①hHSFB②hHSFB with CTGF, MTT were used to detect proliferation,western-blot were used to detect a- SMA which represented differentiation and to detect STATs to learn their relationship. Results In the premise that proliferation and differentiation of group 2 was much higher than that of group 1 (P〈0.05), western-blot was used to find out that the quantity of activated STAT1 in group 2 was much higher than that in group 1 (P〈0.01). STAT2-6 were activated to some extent, but we couldn't find the same rules with STAT1. Conclusion STAT1 may be important in the process of CTGF-induced proliferation and differentiation of hHSFB.The results above may afford new direction to inhibit scar fibrosis and contraction.