病理性周期性张应力诱导人牙周膜细胞凋亡的机制研究  

Mechanism of Pathology Cyclic Strain-induced Apoptosis in Human Periodontal Ligament Cells

作　　者：王莉[1] 汪廷乐 孟冉[1] 唐天鸿 宋萌[1] 潘劲松[1] 

机构地区：[1]上海交通大学附属第一人民医院口腔科,上海200080 [2]上海市闵行区中心医院口腔科,上海201100

出　　处：《现代生物医学进展》2015年第22期4210-4213,4224,共5页Progress in Modern Biomedicine

基　　金：国家自然科学基金项目(11172177);上海交通大学医工理交叉基金项目(YG2010MS07)

摘　　要：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。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 mechanism of apoptosis induced by pathology cyclic strain in human PDL cells.

关 键 词：细胞凋亡 人牙周膜细胞 病理性周期性张应力 caspase-3 PARP 

分 类 号：R78[医药卫生—口腔医学]