摘要
目的探讨青蒿素(ART)对β淀粉样蛋白1-42(Aβ1-42)诱导的阿尔茨海默病(AD)模型细胞的影响。方法选择小鼠BV-2小胶质细胞,分为正常对照组、Aβ1-42组、ART组。正常对照组常规培养,Aβ1-42组加入5μmol/L的Aβ1-42制备AD细胞模型,ART组加入8μmol/L的ART及5μmol/L的Aβ1-42。干预24 h后,采用CCK8法检测细胞活力;采用MitoSOX Red特异性探针检测氧化应激水平;采用Real-time PCR检测细胞及上清液炎症因子TNF-α、IL-1β、IL-6水平;采用CYTO-ID自噬染色检测细胞自噬水平,并采用Real-time PCR检测细胞自噬相关蛋白1(Beacline1)及微管相关蛋白轻链3(LC3) mRNA表达水平。结果 Aβ1-42组细胞活力低于正常对照组,ART组细胞活力高于Aβ1-42组(P均<0. 05)。Aβ1-42组MitoSOX荧光强度高于正常对照组,ART组荧光强度低于Aβ1-42组(P均<0. 05)。Aβ1-42组细胞及上清液TNF-α、IL-1β、IL-6水平均高于正常对照组,ART组细胞及上清液TNF-α、IL-1β、IL-6水平均低于Aβ1-42组(P均<0. 05)。Aβ1-42组Beacline1、LC3 mRNA表达均低于正常对照组,ART组Beacline1、LC3 mRNA表达均高于Aβ1-42组(P均<0. 05)。结论 ART能提高AD模型细胞的活性,抑制细胞氧化应激及炎症因子分泌,其机制可能与ART增加自噬激活有关。
Objective To investigate the effect of artemisinin (ART) on β-amyloid 1-42 (Aβ1-42)-induced Alzheimer's disease (AD) model cells. Methods Mouse BV-2 microglia cells were divided into the control group, Aβ1-42 group, and ART group. The cells in the control group were routinely cultured, 5 μmol/L Aβ1-42 was added to the Aβ1-42 group, and 8 μmol/L ART and 5 μmol/L Aβ1-42 were added to the ART group. After 24 h of intervention, the cell viability was detected by CCK8. The oxidative stress level was detected by MitoSOX Red specific probe. The real-time PCR was used to detect the expression levels of inflammatory factors such as tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β) and interleukin-6 (IL-6) in cells and supernatants. The autophagic activity was detected by CYTO-ID autophagy detection kit, and the expression levels of autophagy-related protein 1 (Beacline1) and light chain 3 (LC3) mRNA were detected by real-time PCR. Results The cell viability of the Aβ1-42 group was lower than that of the control group, and the cell viability of the ART group was higher than that of the Aβ1-42 group (all P <0.05). The fluorescence intensity of MitoSOX in the Aβ1-42 group was higher than that in the control group, and the fluorescence intensity in the ART group was lower than that in the Aβ1-42 group (all P <0.05). The expression levels of TNF-α, IL-1β, and IL-6 in cells and supernatants of the Aβ1-42 group were higher than those in the control group. The expression levels of TNF-α, IL-1β, and IL-6 in the cells and supernatant of the ART group were lower than those in the Aβ1-42 group (all P <0.05). The expression levels of Beacline1 mRNA and LC3 mRNA in the Aβ1-42 group were lower than those in the control group. The expression levels of Beacline1 mRNA and LC3 mRNA in the ART group were higher than those in the Aβ1-42 group (all P <0.05). Conclusion ART can increase the activity of AD model cells, inhibit cell oxidative stress and inflammatory factor secretion, and its mechanism may be related t
作者
龙惠萍
石胜良
王成志
LONG Huiping;SHI Shengliang;WANG Chengzhi(Guangxi Medical University, Nanning 530031, China)
出处
《山东医药》
CAS
2019年第11期5-8,共4页
Shandong Medical Journal
基金
国家自然科学基金资助项目(81460183)
关键词
阿尔茨海默病
青蒿素
氧化应激
炎症
自噬
Alzheimer's disease
artemisinin
oxidative stress
inflammation
autophagy
