灵芝多糖对Aβ25-35诱导的PC12细胞损伤的保护性研究

目的观察灵芝多糖(GLP)对β-淀粉样蛋白(Aβ25-35)诱导的PC12细胞损伤的保护作用。方法将Aβ25-35或(和)不同浓度的GLP加入体外培养的PC12细胞中,用MTT检测PC12细胞活力的变化;以DCFH-DA来检测细胞内活性氧(ROS)水平的改变;通过Western Blotting来检测Bcl-2和Bax的表达水平。结果 Aβ25-35处理36h后的PC12细胞存活率仅为对照的60.7%,细胞内ROS水平上升到原来的222.7%,同时Bcl-2/Bax比值下降,为对照组的60.0%。经不同浓度的GLP预处理后,细胞存活率均显著提高,分别能达到69.7%,80.7%和88.3%(P<0.01);10g/ml GLP预处理PC12细胞24h后,细胞内ROS水平下降至正常组的160.6%,Bcl-2/Bax比值升高到93.6%,P值均<0.01。结论 GLP对Aβ25-35诱导的PC12细胞损伤有保护作用。

Protective effect of ganoderma lucidum polysaccharide against-amyloid-induced neurotoxicity in PC12 cells

Objective To observe the protection effects of ganoderma lucidum polysaccharide(GLP)on-amyloid(A)induced neurotoxicity in PC12 cells.Methods Neurotoxicity was induced by addition of Aβ25-35 into cultures of PC12 cells and different doses of GLPS were administrated 2h before addition of Aβ25-35 into PC12 cell cultures.Cell viability,ROS level and the expression of Bcl-2 and Bax were measured using MTT,DCFH-DA and western blotting,respectively.Results The percentage of viability of PC12 cells treated with Aβ25-35 for 36h was 60.7% of control group.In addition,treatment with Aβ25-35 increased cellular ROS level(222.7% of the control value)and reduced the ratio of Bcl-2/Bax(60.0% of the control value).Pretreatment with single dose of GLP at 2,10,and 50 μg/ml increased cell viability by 65%,80.7%,and 88.3%(P<0.01),respectively.In parallel,treatment with GLP at 10 μg/ml significantly decreased the level of intracellular ROS(160.6% of the control value)and moderated the ratio of Bcl-2/Bax(93.6% of the control value),all P value<0.01.Conclusion The results suggest that pretreatment of GLP protects PC12 cells against Aβ25-35 induced neurotoxicity.