玉郎伞多糖对β淀粉样蛋白所致PC12细胞损伤的影响

The effects of Yulangsan polysaccharide on PC12 cells injury induced by Aβ_(25-35)

目的探讨玉郎伞多糖(YLSP)对β淀粉样蛋白(βamyloid pepitide,Aβ25-35)损伤大鼠肾上腺髓质嗜铬细胞瘤细胞(PC12细胞)的保护作用。方法取对数生长期的PC12细胞分为6组:空白对照组、Aβ25-35模型组、阳性对照药组、不同浓度(0.01,0.1,1.0μg.ml-1)YLSP处理组,各组按要求处理后收集细胞进行检测。MTT比色法分析细胞存活率,试剂盒检测细胞培养上清液LDH水平,流式细胞仪检测细胞内活性氧簇(ROS)及线粒体膜电位(MMP)水平。结果 MTT显示YLSP处理组细胞存活率明显高于Aβ25-35模型组(P<0.01);细胞损伤模型组细胞培养液中LDH及细胞内ROS水平均较正常对照组高(P<0.05或P<0.01),MMP水平较正常对照组低(P<0.01),YLSP各剂量组细胞培养液中LDH及细胞内ROS水平均较模型组低(P<0.05或P<0.01),MMP水平除低剂量组外,均较模型组高(P<0.05或P<0.01)。结论 YLSP对Aβ25-35诱导的PC12细胞损伤有保护作用。

Objective To investigate the protective effects of YLSP on Aβ25-35 induced injury in PC12 cells. Methods Cultured PC12 cells were divided into 6 groups:control group,Aβ25-35 treated model group,positive control drug group,0.01,0.1,1.0μg·mL-1 YLSP treated groups.MTT assay was employed to analyze the PC12 cell viability.After pretreated with YLSP,the content of LDH in culture supernatant was examined by kits,The mitochondrial membrane potential(MMP) was analyzed by rhodamine 123 stain FCM.The level of reactive oxygen species(ROS) in PC12 cells was measured by dihydrohodamine 123 stain FCM. Results β-Amyloid peptide 25-35(Aβ25-35) induced a decrease in viability(P<0.01) and an increase of LDH release of PC12 cells(P<0.01) along with dissipation of MMP(P<0.01) as well as well overproduction of ROS(P<0.01).When PC12 cells were co-treated with YLSP and Aβ25-35,a decrease in viability of PC12 cells induced by 10μM Aβ25-35 was blocked by YLSP(P<0.01).YLSP also decreased the release of LDH(P<0.05) and inhibited the dissipation of MMP(P<0.05 or P<0.01) and overproduction of ROS(P<0.05 or P<0.01). Conclusion YLSP can protect PC12 cells from injury induced by Aβ25-35,which may be associated with the overproduction of ROS induced by Aβ25-35.