缺氧条件下右美对胶质瘤细胞活性的影响

Effects of Dextromethorax on Glioma Cell Activity under Hypoxia

该研究探究右美托咪定(dexmedetomidine,右美,Dex)在常氧和缺氧条件下对U87胶质瘤细胞增殖、凋亡、迁移和侵袭的影响。用氯化钴(CoCl2,400μmol/L)模拟缺氧条件,利用CCK-8观察在常氧和缺氧条件下,不同浓度的右美(0、5、10、20、40、80μmol/L)在不同时间点(24、48、72 h)对U87胶质瘤细胞增殖的影响,流式细胞术检测细胞凋亡水平和细胞周期变化,Transwell检测细胞迁移和侵袭能力的变化,采用Western blot检测各对应蛋白的变化情况。结果显示,缺氧处理可抑制右美对U87的促增殖和抗凋亡作用,但是会促进右美对U87迁移和侵袭能力的提升。缺氧处理后AKT磷酸化水平降低,ERK1/2磷酸化水平升高,周期蛋白和凋亡蛋白也出现部分变化。此外,在缺氧条件下右美促进MMP7和MMP9的表达。综上,缺氧抑制右美对胶质瘤细胞的促增殖和抗凋亡作用,但会辅助右美促进细胞迁移和侵袭。

The aim of the study was to investigate the effects of Dexmedetomidine on proliferation,apoptosis,migration and invasion of U87 glioma cell under hypoxic and normoxic conditions.Cobalt chloride(CoCl2,400μmol/L)was used to simulate hypoxia conditions.The study observed the proliferating effect of Dexmedetomidin at different concentrations(0,5,10,20,40,80μmol/L)during different time(24,48,72 h)on U87 glioma cells under normoxia and hypoxia by CCK-8,and flow cytometry was used to detect cell apoptosis and cell cycle changes.Migration and invasion abilities were detected by Transwell.Western blot was used to detect the changes of each proteins.Results showed that hypoxia treatment inhibited the proliferative and anti-apoptotic effects of Dexmedetomidine on U87,but promoted the migration and invasion of Dexmedetomidine on U87.After hypoxia treatment,the phosphorylation level of AKT was decreased.The phosphorylation level of ERK1/2 was increased,and the cyclins and apoptotic proteins were also partially changed.In addition,Dexmedetomidine promoted the expression of MMP7 and MMP9 under hypoxia.In conclusion,hypoxia inhibits the pro-proliferation and anti-apoptotic effects of Dexmedetomidine on glioma cells,but assists Dexmedetomidine in promoting cell migration and invasion.