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首页|期刊导航|中国美容医学|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

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OACSTPCD

The Role and Mechanism of 2-APB Inhibits the Apoptosis of Condylar Chondrocytes Induced by Static Pressure

中文摘要英文摘要

目的:探讨TRPM7抑制剂2-APB对静压力诱导的髁突软骨细胞凋亡抑制作用及其机制.方法:通过胰蛋白酶消化法提取大鼠髁突软骨细胞,施加不同条件静压力条件,给予不同条件2-APB干预后,以Flou-3AM荧光探针检测胞内钙离子浓度,以流式细胞术检测细胞凋亡率,以Western Blot检测p38蛋白表达,以RT-PCR检测P38mRNA表达水平.进一步采用p38抑制剂进行干预处理,分析细胞凋亡情况变化.结果:不同压力条件下细胞内钙离子浓度与细胞凋亡率变化趋势高度一致,Pearson相关系数值为0.916(P<0.01),有着显著的正相关关系.2-APB可明显抑制静压力诱导的胞内钙离子浓度增高(P<0.01);2-APB与BAPTA-AM对胞内钙离子浓度抑制效果差异无统计学意义(P>0.05).2-APB可明显抑制静压力诱导的细胞凋亡率升高及p38蛋白、mRNA高表达(P<0.01).SB203580可明显抑制静压力诱导的细胞凋亡率升高(P<0.01).结论:2-APB对静压力诱导的髁突软骨细胞凋亡有抑制作用,其机制可能与抑制TRPM7有关.静压力作用下TRPM7介导的钙离子增高是引发细胞凋亡损伤的途径,p38在其中发挥了重要作用,抑制TRPM7介导的钙离子内流可能成为缓解压力诱导细胞损伤的途径.

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.

古扎丽努尔·阿巴拜克力;肖朋

新疆医科大学第七附属医院口腔科 新疆 乌鲁木齐 830028新疆医科大学第七附属医院口腔科 新疆 乌鲁木齐 830028||新疆医科大学第二附属医院口腔科 新疆乌鲁木齐 830063

口腔医学

静压力髁突软骨TRPM7p38通道细胞凋亡

static pressurecondylar cartilagetrpm7p38 channelapoptosis

《中国美容医学》 2024 (010)

7-12 / 6

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)

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