牵张应变诱导人牙周膜细胞凋亡信号通路初探

摘要

Objective To explore the apoptosis mechanism of human periodontal ligament cells ( HPDLCs) induced by Caspase un⁃der stretching force. Methods HPDLCs were cultured in vitro, and cells were stretched by dynamic mechanical strain 1%, 10% and 20% for 6 h, 12 h, 24 h and 48 h. The Caspase⁃3 activity was measured after stretching in PDL cells that were treated with a specific inhibitor of either Caspase⁃8 or Caspase⁃9 prior to the application of stretching force. Results The activity of Caspase⁃3 increased sub⁃stantially in a time and force dependent manner after the application of a cyclic stretching force. It reached a peak at 24 h. The Caspase⁃9 inhibitor abolished the stretching force⁃induced activation of Caspase⁃3, whereas the Caspase⁃8 inhibitor demonstrated no effect. Con⁃clusion Cyclic stretching force can induce apoptosis in HPDLCs through the activation of Caspase⁃3 via the Caspase⁃9 signaling cas⁃cade.%目的：通过研究Caspase酶在牵张应变作用下的变化，来初步探讨其引起人牙周膜细胞（ HPDLCs）凋亡的可能机制。方法体外培养HPDLCs，利用动态机械应变细胞加载装置对HPDLCs加载1％、10％和20％的动态牵张应变6、12、24、48 h，利用酶标仪检测Caspase⁃3活性以及添加Caspase⁃8和Caspase⁃9阻断剂后Caspase⁃3活性。结果 Caspase⁃3活性具有一定的时间和应变值依赖性，各应变组细胞的Caspase⁃3活性在加载24 h时达到峰值，Caspase⁃9阻断剂可以显著降低Caspase⁃3的活性，而Caspase⁃8却并没有明显作用同时发现。结论 Caspase⁃9激活Caspase⁃3介导的凋亡通路参与了牵张应变诱导HPDLCs的凋亡。