摘要
目的:探讨机械力对盆底成纤维细胞双向作用。方法:收集2013年1月到2015年1月于我院因非盆腔器官脱垂患者行阴式全子宫切除的骶主韧带组织,原代培养成纤维细胞,根据机械力加载参数不同进行如下分组:(1)不加力对照组;(2)1mm 4h0.5Hz组;(3)4mm 4h0.5 Hz组。CCK-8法检测各组加力干预后细胞增殖活性,Western Blot检测各组细胞中Ⅰ、Ⅲ型胶原蛋白的表达。结果:不同力学参数加载人盆底成纤维细胞后,与对照组相比,1 mm 4h0.5 Hz组细胞增殖活性增强(188.22%±10.53%),4 mm 4h0.5 Hz组细胞增殖活性减弱(66.09%±4.06%),差异均有统计学意义(P<0.05)。Western Blot检测各组中Ⅰ、Ⅲ型胶原蛋白表达水平的变化,与对照组相比,1mm 4h0.5 Hz组的人盆底成纤维细胞Ⅰ、Ⅲ型胶原蛋白的表达明显上调(P<0.05,P<0.001),而4mm 4h0.5Hz组的人盆底成纤维细胞Ⅰ型胶原蛋白的表达明显下调(P<0.001,P<0.05)。结论:机械力对盆底组织有损伤或修复的双向调控作用,其机制可能为机械力对盆底成纤维细胞具有促增殖或损伤双向调控作用,并双向调控Ⅰ、Ⅲ型胶原蛋白代谢。
Objective:To investigate the dual effect of mechanical strain on the pelvic fibroblast cells.Methods:Specimens were taken from uterosacral ligament and cardinal ligament complexes,fibroblasts were primary cultured and purified as described previously.Depending on the mechanical stretch parameters,three experimental groups were set up:(1)Control group:0 mm 0 h0 Hz group,(2)1 mm 4 h0.5 Hz group,and(3)4 mm 4 h0.5 Hz group.Cell counting kit-8(CCK-8)was used to detect cell growth and viability.Western Blotting was used to evaluate the expression of COL1 A1 and COL3 A1.Results:The results of CCK-8 showed a significantly higher viability of pelvic fibroblast cells in 1 mm 4 h0.5 Hz group,but a lower viability in 4 mm 4 h0.5 Hz group as compared with the control group(P<0.05).The results of Western Blotting showed a significantly higher expression of COL1 A1 and COL3 A1 in 1 mm 4 h0.5 Hz group(P<0.05,P<0.001),but the expression of COL1 A1 and COL3 A1 in 4 mm 4 h0.5 Hz group were lower than in control group(P<0.001,P<0.05).Conclusion:The mechanical stretch plays a dual effect on pelvic support fibroblasts.The mechanism may be that moderate mechanical stretchstimulates fibroblast cells proliferation and up-regulates the expression of collagen,but excessive mechanical stretch will injure fibroblast cells and down-regulate the expression of collagen.
出处
《武汉大学学报(医学版)》
CAS
2018年第3期365-368,共4页
Medical Journal of Wuhan University
基金
国家自然科学基金面上项目(编号:81471442)
中央高校基本科研业务费专项资金资助项目(编号:2042016kf0120)
湖北省自然科学基金资助项目(编号:2017CFB750)