病理性周期性张应力诱导人牙周膜细胞凋亡的机制研究

目的:阐明病理性周期性张应力诱导人牙周膜细胞凋亡的分子机制。方法:人牙周膜细胞取自健康前磨牙,经过3?5代传代,细胞受到20%牵张力,时间为6 h或24 h,通过用膜联蛋白异硫氰酸荧光素(V-FITC)和碘化丙啶(PI)结合流式细胞仪检测细胞凋亡,用Western Blot法研究caspase-3,cleaved caspase-3,116 kDa PARP-1和85 k Da PARP-1蛋白的表达变化。结果:人PDL细胞受到病理性周期性张应力时存在凋亡,并以一种时间依赖的方式增加。受到病理性周期性张应力后裂解的caspase-3和PARP蛋白随着时间增加,然而抑制caspase-3的活性却可以抑制细胞的凋亡,但并不能抑制由其他通路导致的凋亡。结论:病理性周期性张应力通过caspase-3/PARP途径诱导人牙周膜细胞的凋亡。

Mechanismof Pathology Cyclic Strain-induced Apoptosis in Human Periodontal Ligament Cells

Objective:To elucidate the molecular mechanisms by which pathology cyclic strain induces the apoptosis of human periodontal ligament (PDL) cells.Methods:The human PDL cells were obtained from healthy premolars. After three to five passages, the cells were stretched by 20 % strain for 6 h and 24 h, then the apoptosis were detected through annexin fluorescein isothiocyanate (V-FITC) and propidium iodide (PI) binding by flow cytometry, and the protein expression of caspase-3 and PARP was investigated by Western Blot.Results:Human PDL apoptotic cells were increased in a time-dependent manner in response to pathology cyclic strain. Cleaved caspase-3 and PARP protein was increased by pathology cyclic strain along with time. Furthermore, inhibition of caspase-3 prevented stretch-induced apoptosis but did not prevent all apoptosis caused by other signaling pathways.Conclusion:Our results suggested that pathology cyclic strain induced apoptosis in human PDL cells through caspase-3/PARP pathway. Our findings may provide a novel insight into the mechanismof apoptosis induced by pathology cyclic strain in human PDL cells.