p38丝裂原激活蛋白阻断剂对机械压力诱导人牙周膜成纤维细胞表达白介素-6的影响

Effects of p38 inhibitor on expression of IL-6 stimulated by mechanical pressure in HPLF

目的分析p38丝裂原激活蛋白(MAPK)在压力诱导人牙周膜成纤维细胞(HPLF)合成炎症因子白介素(IL)-6过程中所起的作用。方法以p38MAPK阻断剂SB203580对HPLF预处理60min,然后用酶联免疫吸附法检测HPLF受200kPa压力刺激后培养上清内IL-6蛋白水平,比较预处理组与对照组2之间IL-6含量的差异。结果加压后16和24h两时间点加力组均较对照组1IL-6表达量显著增高;而预处理组较对照组2IL-6表达量下降。结论p38MAPK是机械压力诱导HPLF产生IL-6的重要环节。

Objective To investigate the role of p38 MAPK of human periodontal ligament fibroblasts(HPLF) in the expression of inflammatory cytokine IL-6 subjected to mechanical pressure, and to explore the mechanisms of the occlusal trauma injury to periodontium. Methods We pretreated HPLF with SB203580 for 60 minutes, and then examined the differences of protein levels of IL-6 between pretreated group and the 2nd control group induced by 200 kPa mechanical pressure. IL-6 both in the cell and culture media were measured by enzyme-linked immunosorbent assay (ELISA). Results In comparison with the 1st control group, the level of IL-6 in pressure group was highly increased at 16 h and 24 h, but the level of IL-6 in pretreated group was lower than that in the 2nd control group. Conclusion p38 MAPK of HPLF acts as an important cooperative factor to regulate IL-6 synthesis induced by mechanical pressures.