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作 者:陈红淑[1] 杨元宵[2] 冯耀荣[3] 许亚萍[1] 郑敏霞[1]
机构地区:[1]浙江中医药大学附属第一医院,浙江杭州310006 [2]浙江中医药大学药学院,浙江杭州310053 [3]浙江中医药大学附属第二医院,浙江杭州310005
出 处:《中华中医药学刊》2015年第7期1679-1681,I0012,共4页Chinese Archives of Traditional Chinese Medicine
基 金:浙江省教育厅项目(Y201431211);全国名老中医药专家传承工作室建设项目
摘 要:目的:观察人参皂苷Rg1对β-淀粉样蛋白(beta-Amyliod,Aβ1-42)诱导PC12细胞自噬性死亡的作用,试探究其神经保护机制。方法:将PC12细胞分为对照组、Aβ组和Aβ+Rg1组。Aβ组细胞用Aβ1-42(10μmol/L)处理24 h;Aβ+Rg1组细胞分别用12.5、25、50μmol/L Rg1预处理24 h后,加入Aβ1-42(10μmol/L)继续培养24 h。采用MTT法测定各组细胞活力,免疫荧光染色法检测细胞自噬相关蛋白LC3-Ⅱ表达变化,Western blot法检测LC3-Ⅱ和Beclin-1蛋白表达变化。结果:对照组比较,Aβ组细胞活力显著下降(P<0.01);与模型组比较,Rg1各剂量组细胞活力显著高于Aβ组(P<0.01)。与对照组比较,Aβ组LC3-Ⅱ和Beclin-1蛋白表达显著上升(P<0.01);与模型组比较,Rg1各剂量组LC3-Ⅱ和Beclin-1蛋白表达显著低于Aβ组(P<0.01)。结论:人参皂苷Rg1可能通过抑制Aβ诱导的细胞自噬性死亡发挥神经保护作用。Objective:Ginsenoside Rgl ,one of the tfiologieally active ingredients of ginseng,may be a candidate neuro- protective drug. In the present study,the meehanism underlying the neuroproteetiun provided by ginsenosde Rgl was stud- led against aulophagy induced by Aβ1 -42 in PC12 eells. Method: PC12 cells were divided into Aβ group, Aβ + Rgl group and e.ontrol group. Ceils in Aβ group were treated with Aβ1 -42 ( 10 μmol/L) for 24 h, and cells in Rgl group were pre - incubated with Rgl ( 12.5,25,50 μ mol/l,) for 24 h prior to treatment with 10 μmol/L Aβ1 -42 for 24 h, Cell viability was detected by MTT;The protein expression of LC3 - Ⅱ protein was assayed by lmmunotlnoreseence; Western blotting was used to detect the expression of LC3 - 11 and Beclin - 1. Results:The results showed that the viability of PCI2 cells in Aβ group was significantly lower than thai in control group ( P 〈 0. 01 ) , and the viability of PCI2 cells in Rgl group was significantly higher than that in Aβ group( P 〈 0.05). Rgl effectively inhibited the expression of LC3 - lI and Beelin - I protein induced by Aβ -42. Conclusion:These results suggest that Rgl exhibits neuroproteetive effect through inhibiting Aβ- induced autophagy in PCI2 cells.
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