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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 mechanism of apoptosis induced by pathological cyclic tensile stress in human periodontal ligament cells. METHODS: Human periodontal ligament cells were obtained from healthy premolar and passaged for 3 to 5 passages. The cells were exposed to 20% strain for 6 h or 24 h. The cells were cultured with Annexin V-fluorescein isothiocyanate (V-FITC ) And propidium iodide (PI) were detected by flow cytometry. The expression of caspase-3, cleaved caspase-3, 116 kDa PARP-1 and 85 kDa PARP-1 protein were detected by Western Blot. RESULTS: Human PDL cells were apoptoticly exposed to pathological cyclic tensile stress and increased in a time-dependent manner. The caspase-3 and PARP proteins cleaved by pathological cyclic tensile stress increased with time, however, inhibition of caspase-3 activity inhibited cell apoptosis but did not inhibit apoptosis induced by other pathways. CONCLUSION: Pathological cyclic tensile stress induces apoptosis of human periodontal ligament cells through the caspase-3 / PARP pathway.