目的 探讨模拟正畸静压力刺激牙周膜干细胞增殖的TGFβ/STAT信号通路参与机制,为相关研究提供参考。方法 体外培养牙周膜干细胞至生长状态良好后加压处理(100 kPa)不同时间(1、6、12 h),Western blotting法检测细胞凋亡相关蛋白及TGFβ/STAT信号通路蛋白的表达。结果 体外培养的牙周膜干细胞具有多向分化能力,加压处理1 h和6 h后细胞Bax明显增强(0.34±0.05 vs 0.42±0.08, P<0.05)而Bcl-2水平明显减弱(0.33±0.05 vs 0.29±0.05, P<0.05),TGFβ/STAT信号通路蛋白TGFβ(0.34±0.06 vs 0.39±0.07, P<0.05)及STAT2表达明显增强(0.32±0.06 vs 0.43±0.08, P<0.05),而处理12 h干细胞的上述蛋白表达差异无统计学意义(P>0.05)。结论 模拟正畸静压力刺激可明显抑制体外培养的牙周膜干细胞的增殖过程,其可能与TGFβ/STAT信号通路异常有关。

Objective To analyze the mechanism by which TGF beta/STAT signaling pathway is involved in simulating the proliferation of periodontal ligament stem cells stimulated by orthodontic static pressure.Methods The periodontal ligament stem cells were cultured in vitro to grow well before being pressed (100 KPa, 1 H, 6 h and 12 h) for different lengths of time. Western blotting was used to detect the expressions of apoptosis related proteins and TGF/STAT signaling pathway proteins.Results In vitro cultured human periodontal ligament stem cells had multiple differentiation abilities. After 1 h and 6 h of treatment with pressure, the Bax increased significantly (0.34±0.05 vs 0.42±0.08, P<0.05), while the level of Bcl2 decreased significantly (0.33±0.05 vs 0.29±0.05, P<0.05). The expressions of TGF beta/STAT signaling protein TGF beta (0.34±0.06 vs 0.39±0.07, P<0.05)and STAT2 increased significantly(0.32±0.06 vs 0.43±0.08, P<0.05). There was no significant difference in the expressions of these proteins in stem cells treated for 12 hours (P>0.05).Conclusion Simulated orthodontic static pressure stimulation can significantly inhibit the proliferation of periodontal ligament stem cells in vitro, which may be related to abnormality of TGF beta/STAT signaling pathway.