Schizandrin A ameliorates cognitive functions via modulating microglial polarisation in Alzheimer's disease mice

被引:20
|
作者
Wang, Qi [1 ]
Liu, Li [2 ]
Guan, Huibo [1 ]
Zhou, Yanyan [1 ]
Li, Quan [3 ]
机构
[1] Heilongjiang Univ Chinese Med, Teaching & Res Dept Basic Theory Tradit Chinese M, Harbin, Heilongjiang, Peoples R China
[2] Heilongjiang Univ Chinese Med, Affiliated Hosp 1, Dept Cardiovasc Dis, Harbin, Heilongjiang, Peoples R China
[3] Heilongjiang Univ Chinese Med, Affiliated Hosp 1, Hosp Off, Harbin, Heilongjiang, Peoples R China
关键词
Microglial cells; apoptosis; cognitive disorder; SCHISANDRIN; INFLAMMASOME; MECHANISMS; THERAPY; MODEL; M1;
D O I
10.1080/13880209.2021.1941132
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Context Schizandrin A (Sch A) is a major phytochemical from Schisandra chinensis (Turcz.) Baill. (Schisandraceae), which exerts a neuroprotective effect in Alzheimer's disease (AD). Objective To investigate the mechanism of Sch A in AD. Materials and methods AD group: APP/PS1 transgenic mice served as AD models; AD + SCH group: APP/PS1 received 2 mg/kg Sch A by intragastric administration; WT: C57BL/6 mice were used as control. For in vitro assay, mouse microglial BV2 cells were treated with 0.5 mu g/mL lipopolysaccharide or combined with 10 mu mol/L Sch A for 24 h. The cognitive function and apoptosis in the mice was estimated. Microglial polarisation in the mice and cells was analysed. Results Sch A treatment effectively improved spatial learning and memory ability and suppressed apoptosis in the brain tissues of APP/PS1 mice. APP/PS1 mice exhibited an increase in the levels of A beta 1-42 (2367.9 +/- 431.1 pg/mg) and A beta 1-40 (1753.3 +/- 253.4 pg/mg), which was abolished by Sch A treatment. Moreover, Sch A treatment repressed the proportions of iNOS(+)/Iba-1(+) cells and IL-6 expression, while enhanced the proportions of Arg-1(+)/Iba-1(+) cells and IL-10 expression in APP/PS1 mice. In vitro, Sch A treatment reduced the proportions of CD16/32(+) cells, iNOS expression and IL-6 levels (25.7 +/- 5.3 pg/mL) repressed M1 polarisation, and enhanced the proportions of CD206 cells, Arg-1 expression and IL-10 levels (75.9 +/- 12.8 pg/mL) in BV2 cells. Conclusions This research confirms the neuroprotective effect of Sch A in AD, suggesting that Sch A may become a potential anti-AD agent.
引用
收藏
页码:860 / 867
页数:8
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