不同静水压力对大鼠髁突软骨细胞的TRPM7和Fas蛋白表达的影响

The Effect for the Expression of Fas and TRPM7 Protein under Different Hydrostatic Pressure in MCCs

目的:观察不同静水压力作用下大鼠颞下颌关节髁突软骨细胞TRPM7和Fas蛋白的表达情况,探讨不同静水压力可能对软骨细胞凋亡的影响。方法:将软骨细胞随机分组,分别给予不同大小和时间的压力刺激。Western Blot检测每组TRPM7和Fas蛋白量。结果:加压时间为1h、2h时,6~10kPa实验组的Fas蛋白量均低于对照组,差异具有统计学意义,P<0.05;当压力值为20kPa/2h、30kPa/1h或2h时,实验组高于对照组,差异具有统计学意义,P<0.05;当压力为20kPa/1h时,实验组高于对照组,差异无统计学意义,P>0.05。加压时间分别为1h、2h时,6~20kPa实验组的TRPM7蛋白量均低于对照组,差异具有统计学意义,P<0.05;当压力值为30kPa/2h时,实验组高于对照组,差异具有统计学意义,P<0.05;但压力值为30kPa/1h时,实验组高于对照组,差异无统计学意义,P>0.05。结论:较小压力范围内,可能抑制软骨细胞的凋亡;压力条件超过一定界限后,可能对软骨细胞凋亡有促进作用。

Objective To observe the expression of Fas and TRPM7 protein under different hydrostatic pressure in mandibular condylar cartilage cells. To explore the effect of different hydrostatic pressure on cartilage cell apoptosis. Methods Divided MCCs into different groups randomly. Different hydrostatic pressure and duration were given to MCCs. The expression of TRPM7 and Fas protein was detected by Western Blot to observe the change of apoptin under different pressure and duration in vitro. Results The Fas protein in experimental group expressed less than control group with the pressure （6kPa, 8kPa, 10kPa） under the duration of lh, or 2h, the difference is statistically significant（P〈0.05）. Fas protein expressed much more than control control group （20kPa/2h, 30kPa/lh, 30kPa/2h）, P〈0.05. When the pressure was 20kPa/lh, the difference is not statistically significant（P〉0.05）. The expression of TRPM7 protein in experimental group expressed less than control group with the pressure （6kPa, 8kPa, 10kPa, 20kPa） under the duration of lh or 2h, P〈0.05. TRPM7 protein expressed more than control group under the pressure of 30kPa/2h, P〈0.05. But the group of 30kPa/lh was not, P〉0.05. Conclusion Within a scope of a certain pressure and time, the condition might inhibited the apoptosis of MCCs. Above the scope of the certain pressure or time, it maight promote the apoptosis. The study laid the theoretical foundation for researching pathological mechanism of TMD.