五味子醇甲通过Aβ_(25-35)诱导PC12细胞损伤对氧化应激及炎症因子的影响

Effects of schisandrin A on regulation of Aβ_(25-35)-induced PC12 cell oxidative stress and inflammatory factors

目的探讨五味子醇甲(SCH A)通过Aβ_(25-35)诱导PC12细胞损伤对氧化应激及炎症因子的影响。方法CCK8、流式细胞仪联合检测,设立20μmol/L Aβ_(25-35)诱导PC12建立细胞损伤模型。MTT、流式细胞仪确立10μg/mL SCH A为本次实验药物剂量。实验分为空白组、模型组(20μmol/L Aβ_(25-35))和SCH A组(10μg/mL SCH A+20μmol/L Aβ_(25-35))。试剂盒检测超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽(GSH)表达水平;Western blot检测白介素-1β(IL-1β)、白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)蛋白水平。结果10μg/mL SCH A能显著提高SOD[(17.12±0.33)μ/mg比(10.02±0.12)μ/mg,P<0.01]、GSH[(12.32±0.73)μmol/g比(6.83±0.73)μmol/g,P<0.01]水平,降低MDA[(3.73±0.25)μmol/mg比(6.77±0.25)μmol/mg,P<0.01]水平;降低IL-1β[(4.25±0.61)μg/μL比(6.28±0.72)μg/μL,P<0.01]、IL-6[(2.18±0.25)μg/μL比(4.80±0.76)μg/μL,P<0.01]、TNF-α[(2.59±0.15)μg/μL比(4.53±0.39)μg/μL,P<0.01]蛋白表达水平。结论SCH A可能通过降低Aβ_(25-35)诱导PC12细胞的炎性反应,减轻氧化应激,从而发挥细胞保护作用。

Objective To assess the effects of Schisandrin A(SCH A)on Aβ_(25-35)-induced PC12 cell oxidative stress and inflammatory factors and the underlying molecular events.Methods Aβ_(25-35)(20μmol/L)was added to PC12 cell culture to establish a cell damage model in vitro.Cells were treated with or without 10μg/mL SCH A for cell viability MTT and flow cytometry assays and expression of superoxide dismutase(SOD),malondialdehyde(MDA),and glutathione(GSH).Western blot was used to analyze level of interleukin-1β(IL-1β),interleukin-6(IL-6),tumor necrosis factor(TNF-α).Results Compared to that of control cells,SCH A treatment significantly increased PC12 cell expression of SOD(17.12±0.33 vs.10.02±0.12μ/mg;P<0.01),GSH(12.32±0.73 vs.6.83±0.73μmol/g;P<0.01),but reduced MDA level(3.73±0.25 vs.6.77±0.25μmol/mg;P<0.01),and expression of IL-1β(4.25±0.61 vs.6.28±0.72μg/μL;P<0.01),IL-6(2.18±0.25 vs.4.80±0.76μg/μL;P<0.01),and TNF-α(2.59±0.15vs.4.53±0.39μg/μL;P<0.01).Conclusion SCH A could play a protective role in PC12 cells against Aβ_(25-35)-induced stress and inflammation.