中国美容医学2024，Vol.33Issue(10)：7-12,6.
2-APB抑制静压力诱导髁突软骨细胞凋亡的作用及机制研究
The Role and Mechanism of 2-APB Inhibits the Apoptosis of Condylar Chondrocytes Induced by Static Pressure
摘要
Abstract
Objective To explore the inhibitory effect and mechanism of TRPM7 inhibitor 2-APB on static pressure induced by apoptosis of condylar chondrocytes.Methods The rat condylar chondrocytes were extracted through trypsin digestion method.Different static pressure conditions were administered.After the 2-APB intervention,intracellular calcium concentration was detected by Flou-3AM fluorescence probe.The apoptosis rate was detected by flow cytometry.The expression of p38 protein was detected by Western Blot,and the expression of p38mRNA was detected by RT-PCR.p38 inhibitor was further used to intervene and analyze the changes of cell apoptosis.Results Under different pressure conditions,the change trend of intracellular calcium concentration was highly consistent with that of cell apoptosis rate.The Pearson correlation value was 0.916(P＜0.01),showing a significant positive correlation.2-APB significantly inhibited the increase of intracellular calcium concentration induced by static pressure(P＜0.01).There was no significant difference between 2-APB and BAPTA-AM in inhibiting intracellular calcium concentration(P＞0.05).2-APB could significantly inhibit the increase of cell apoptosis rate and the high expression of p38 protein and mRNA induced by static pressure(P＜0.01).SB203580 could significantly inhibit the increase of cell apoptosis rate induced by static pressure(P＜0.01).Conclusion The increase of calcium ion mediated by TRPM7 under static pressure is the way to cause cell apoptosis injury,and p38 plays an important role in it.Inhibiting TRPM7 mediated calcium ion influx may be a way to alleviate cell apoptosis induced by static pressure.关键词
静压力/髁突软骨/TRPM7/p38通道/细胞凋亡Key words
static pressure/condylar cartilage/trpm7/p38 channel/apoptosis分类
医药卫生引用本文复制引用
古扎丽努尔·阿巴拜克力,肖朋..2-APB抑制静压力诱导髁突软骨细胞凋亡的作用及机制研究[J].中国美容医学,2024,33(10):7-12,6.基金项目
新疆维吾尔自治区自然科学基金-医学联合基金项目(编号:2020D01C182) （编号:2020D01C182）
