中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2014年
38期
3020-3023
,共4页
陆瑜%菅敏钰%熊蔚%韩如泉
陸瑜%菅敏鈺%熊蔚%韓如泉
륙유%관민옥%웅위%한여천
二异丙酚%星形胶质细胞%miR-181a%Bcl-2蛋白
二異丙酚%星形膠質細胞%miR-181a%Bcl-2蛋白
이이병분%성형효질세포%miR-181a%Bcl-2단백
Propofol%Astrocyte%miR-181 a%Bcl-2 protein
目的 探讨丙泊酚通过miR-181a调控Bcl-2蛋白表达对乏糖培养星形胶质细胞的影响.方法 原代培养小鼠星形胶质细胞,使用丙泊酚0、1、5、10、15、20 μmol/L处理12 h,更换乏糖培养24 h后,显微镜下计数星形胶质细胞存活率.观察反应性氧元件(ROS)产生和线粒体膜电位变化的影响;观察miR-181a及Bcl-2蛋白表达水平变化与丙泊酚对星形胶质细胞保护效应的关系.结果 丙泊酚及乏糖处理后,0、1、5、10、15、20 μmol/L丙泊酚处理组星形胶质细胞存活率分别为(0.51±0.03)％、(0.52±0.02)％、(0.52±0.02)％、(0.73±0.04)％、(0.31±0.02)％、(0.21±0.02)％,差异有统计学意义(F=118.62,P＜0.001);其中10 μmol/L丙泊酚处理组高于0μmol/L丙泊酚处理组,15 μmol/L及20 μmol/L丙泊酚处理组低于0μmol/L丙泊酚处理组.10 μmol/L丙泊酚可以明显改善乏糖引起的氧化应激反应,增加线粒体膜电位稳定性.Bcl-2蛋白表达在10 μmol/L丙泊酚处理后明显升高,同时,miR-181a表达明显降低.结论 10 μmol/L丙泊酚对乏糖培养星形胶质细胞具有保护作用,与其抑制miR-181a并增强Bcl-2蛋白表达有关.
目的 探討丙泊酚通過miR-181a調控Bcl-2蛋白錶達對乏糖培養星形膠質細胞的影響.方法 原代培養小鼠星形膠質細胞,使用丙泊酚0、1、5、10、15、20 μmol/L處理12 h,更換乏糖培養24 h後,顯微鏡下計數星形膠質細胞存活率.觀察反應性氧元件(ROS)產生和線粒體膜電位變化的影響;觀察miR-181a及Bcl-2蛋白錶達水平變化與丙泊酚對星形膠質細胞保護效應的關繫.結果 丙泊酚及乏糖處理後,0、1、5、10、15、20 μmol/L丙泊酚處理組星形膠質細胞存活率分彆為(0.51±0.03)％、(0.52±0.02)％、(0.52±0.02)％、(0.73±0.04)％、(0.31±0.02)％、(0.21±0.02)％,差異有統計學意義(F=118.62,P＜0.001);其中10 μmol/L丙泊酚處理組高于0μmol/L丙泊酚處理組,15 μmol/L及20 μmol/L丙泊酚處理組低于0μmol/L丙泊酚處理組.10 μmol/L丙泊酚可以明顯改善乏糖引起的氧化應激反應,增加線粒體膜電位穩定性.Bcl-2蛋白錶達在10 μmol/L丙泊酚處理後明顯升高,同時,miR-181a錶達明顯降低.結論 10 μmol/L丙泊酚對乏糖培養星形膠質細胞具有保護作用,與其抑製miR-181a併增彊Bcl-2蛋白錶達有關.
목적 탐토병박분통과miR-181a조공Bcl-2단백표체대핍당배양성형효질세포적영향.방법 원대배양소서성형효질세포,사용병박분0、1、5、10、15、20 μmol/L처리12 h,경환핍당배양24 h후,현미경하계수성형효질세포존활솔.관찰반응성양원건(ROS)산생화선립체막전위변화적영향;관찰miR-181a급Bcl-2단백표체수평변화여병박분대성형효질세포보호효응적관계.결과 병박분급핍당처리후,0、1、5、10、15、20 μmol/L병박분처리조성형효질세포존활솔분별위(0.51±0.03)％、(0.52±0.02)％、(0.52±0.02)％、(0.73±0.04)％、(0.31±0.02)％、(0.21±0.02)％,차이유통계학의의(F=118.62,P＜0.001);기중10 μmol/L병박분처리조고우0μmol/L병박분처리조,15 μmol/L급20 μmol/L병박분처리조저우0μmol/L병박분처리조.10 μmol/L병박분가이명현개선핍당인기적양화응격반응,증가선립체막전위은정성.Bcl-2단백표체재10 μmol/L병박분처리후명현승고,동시,miR-181a표체명현강저.결론 10 μmol/L병박분대핍당배양성형효질세포구유보호작용,여기억제miR-181a병증강Bcl-2단백표체유관.
Objective To explore the propofol regulation of Bcl-2 protein expression through miR-181a in glucose deprivation (GD) cultured astrocytes.Methods Primary cultured murine astrocytes were treated with 0,1,5,10,15,20μmol/L propofol for 12 h and then cultured with GD medium for24 h.The cell survival rate was recorded with microscope.Reactive oxygen species (ROS) formation and mitochondrial membrane stabilization were observed.And the expression levels of miR-181a and Bcl-2 protein were recorded to analyze the protection effects of propofol on astrocytes.Results After the treatments of propofol and GD,the survival rates of O,1,5,10,15,20 μmol/L propofol groups were (0.51 ±0.03)％,(0.52±0.02)％,(0.52±0.02)％,(0.73 ±0.04)％,(0.31 ±0.02)％ and (0.21 ±0.02)％.And there were statistical significance (F =118.62,P ＜0.001).Compared with 0 μmol/L propofol group,the survival rate was much higher in 10μmol/L propofol group while much lower in 15 μmol/L and 20 μmol/Lpropofol groups.10 μmoL/L propofol could decrease ROS formation and stabilize mitochondrial membrane.And Bcl-2 protein expression was up-regulated while miR-181a expression inhibited by 10 μmol/L propofol.Conclusion The protection of 10 μmol/L propofol against GD stress in astrocytes is correlated with inhibiting miR-181 a and up-regulating Bcl-2 protein expression.
