摘要
目的探讨人参皂苷Rg1对异氟醚诱导caspase-3活化的影响及其机制。方法通过培养人神经胶质瘤细胞(H4 nave cell)和稳定转染APP基因的细胞(H4-APP cell),给予25μmol/L人参皂苷Rg1预处理12h或者24h后接受异氟醚麻醉。采用蛋白免疫印迹法检测细胞凋亡效应蛋白caspase-3活化程度,利用化学发光法检测5'-三磷酸腺苷(adenosine-5'-triphosphate,ATP)水平的变化,流式细胞仪观察线粒体通透性转运孔(mitochondrial permeability transition pore,m PTP)的开放程度。结果给予25μmol/L人参皂苷Rg1预处理12h,H4 nave细胞及H4-APP细胞的caspase-3活化程度,ATP水平及m PTP开放程度均与异氟醚处理组相比,差异无统计学意义(P>0.05)。延长人参皂苷Rg1预处理时间至24h,H4 nave细胞及H4-APP细胞的caspase-3活化程度,ATP水平及m PTP开放程度均与异氟醚处理组差异有统计学意义(P<0.05)。结论人参皂苷Rg1可能通过保护线粒体功能降低异氟醚诱导caspase-3的活化程度。
Objective To explore the possible beneficial effects and mechanisms of ginsenoside Rg1 on isoflurane-induced caspase-3 activation.Methods We investigated the effects of 25μmol / L ginsenoside Rg1 with 12 h or 24 h pretreated on isoflurane-induced caspase-3 activation in H4 nave and stably-transfected human amyloid precursor protein( APP)( H4-APP cells).For mitochondrial dysfunction,we assessed the mitochondrial permeability transition pore( m PTP) and adenosine-5’-triphosphate( ATP) levels.We employed Western blot analysis,chemiluminescence and flowcytometry.Results Pretreatment with 25μmol / L ginsenoside Rg1 for 12 h did not attenuate the isoflurane-induced caspase-3 activation and mitochondrial dysfunction in H4 nave or H4-APP cells,while pretreatment with 25μmol / L ginsenoside Rg1 for 24 h attenuated the isoflurane-induced caspase-3 activation and mitochondrial dysfunction both in H4 nave and H4-APP cells.Conclusion Ginsenoside Rg1 may ameliorate the isoflurane-induced caspase-3 activation by inhibiting mitochondrial dysfunction.
出处
《医学研究杂志》
2015年第4期52-58,共7页
Journal of Medical Research
基金
北京市科技新星计划基金资助项目(Z131107000413044)