中国骨质疏松杂志

持续静压力通过TRPV4信号通路调控大鼠软骨细胞凋亡

Continuous static pressure regulates apoptosis of rat chondrocytes through the TRPV4 signaling pathway

DOI：10.3969/j.issn.1006-7108.2025.04.007

英文关键词:chondrocytes Static pressure Apoptosis TRPV4 proteins MAPK signaling pathway

基金项目:

作者	单位
梁秋娟1 刘潇1 古丽奴儿·沙吾提1 肖朋2	1.新疆医科大学第五附属医院,口腔科新疆乌鲁木齐 830000 2.新疆医科大学第七附属医院,口腔科新疆乌鲁木齐 830000

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中文摘要:

目的：探讨持续静压力对大鼠软骨细胞凋亡的机制。方法：制备并培养原代大鼠软骨细胞，设置正常对照组、30 KPa压力组、GSK205对照组、GSK205+30 KPa压力组。EdU荧光染色法检测软骨细胞在12 h、24 h和48 h的增殖率。采用流式检测软骨细胞在24 h、48 h和72h的凋亡率。荧光标记测定软骨细胞内48 h时钙离子浓度。免疫印迹法测定软骨细胞TRPV4、JNK、p-JNK、ERK1/2、p-ERK1/2、P38、p-P38蛋白24 h时相对表达水平。结果：与正常对照组比较，30 KPa压力组软骨细胞在各观察时间增殖率均显著减少(P<0.05)；细胞凋亡率均显著增加(P<0.05)；细胞内钙离子荧光强度增强；细胞内TRPV4、磷酸化的JNK、磷酸化的ERK1/2、磷酸化的P38均显著提高(P<0.05)。与30 KPa压力组比较，给予TRPV4的阻断剂GSK205后，GSK205+30 KPa压力组的细胞增殖率显著上升；细胞凋亡率显著减少；细胞内钙离子荧光强度减弱；TRPV4、磷酸化的JNK、磷酸化的ERK1/2、磷酸化的P38均显著减少(P<0.05)。结论：30 KPa持续静压力不仅抑制软骨细胞增殖，还增加软骨细胞凋亡，使细胞内钙离子浓度增加。持续静压力促进大鼠软骨细胞凋亡的可能分子机制为通过TRPV4力学信号感受器激活MAPK信号通路。

英文摘要:

Objective: To investigate the mechanism of sustained static pressure on rat chondrocytes. Method: Rat condylar chondrocytes were isolated and divided into a normal control group, a 30 KPa pressure group, a GSK205 control group, and a 30 KPa pressure+GSK205 group. EDU method was used to measure chondrocyte proliferation at 12, 24, and 48 hours. Flow cytometry was used to measure chondrocyte apoptosis at 24, 48, and 74 hours. Fluorescence probe method was used to detect the intracellular calcium ion concentration in chondrocytes at 48 hours. Western blot was used to determine the protein expression of TRPV4, p-JNK, JNK, p-ERK1/2, ERK1/2, p-P38, and P38 in chondrocytes at 24 hours. Result: Compared with the normal control group, the proliferation rate of cells in the 30 KPa pressure group decreased at all observation times. The apoptosis rate increased significantly. The fluorescence intensity of intracellular calcium ion increased. The TRPV4, phosphorylated JNK, phosphorylated ERK1/2, and phosphorylated P38 proteins in cells increased, and the difference was statistically significant (P<0.05). Compared with the 30 KPa pressure group, the chondrocyte rate in the 30 KPa pressure+GSK205 group was increased. The apoptosis rate decreased in all cases. The fluorescence intensity of intracellular calcium ion decreased. The TRPV4, phosphorylated JNK, phosphorylated ERK1/2, and phosphorylated P38 proteins decreased significantly (P<0.05). Conclusion: Continuous static pressure of 30 KPa on chondrocytes can inhibit cell proliferation, promote apoptosis, and increase intracellular calcium ion concentration. The possible molecular mechanism by which sustained static pressure promotes apoptosis of rat chondrocytes is to activate the MAPK signaling pathway through the TRPV4 mechanical signal receptor.

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