Abstract

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 µg/mL lipopolysaccharide or combined with 10 μmol/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 Aβ1-42 (2367.9 ± 431.1 pg/mg) and Aβ1-40 (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.

中文翻译：

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五味子 A 通过调节阿尔茨海默病小鼠的小胶质细胞极化改善认知功能

摘要

语境

五味子 A (Sch A) 是来自五味子(Turcz.) Baill的主要植物化学物质。（五味子科），在阿尔茨海默病（AD）中发挥神经保护作用。

客观的

研究 Sch A 在 AD 中的作用机制。

材料和方法

AD组：APP/PS1转基因小鼠作为AD模型；AD+SCH组：APP/PS1灌胃给药2 mg/kg Sch A；WT：C57BL/6 小鼠用作对照。对于体外测定，小鼠小胶质细胞 BV2 细胞用 0.5 µg/mL 脂多糖或与 10 µmol/L Sch A 组合处理 24 小时。估计小鼠的认知功能和细胞凋亡。分析了小鼠和细胞中的小胶质细胞极化。

结果

Sch A治疗有效提高了APP/PS1小鼠脑组织的空间学习记忆能力并抑制了细胞凋亡。APP/PS1 小鼠表现出 Aβ1-42 (2367.9 ± 431.1 pg/mg) 和 Aβ1-40 (1753.3 ± 253.4 pg/mg) 水平的增加，这被 Sch A 治疗消除。此外，Sch A 处理抑制了iNOS ⁺ /Iba-1 ⁺细胞的比例和IL-6 表达，同时提高了APP/PS1 小鼠中Arg-1 ⁺ /Iba-1 ⁺细胞的比例和IL-10 的表达。在体外，Sch A 治疗降低了 CD16/32 ⁺的比例 细胞、iNOS 表达和 IL-6 水平 (25.7 ± 5.3 pg/mL) 抑制 M1 极化，并提高 BV2 细胞中 CD206 细胞、Arg-1 表达和 IL-10 水平 (75.9 ± 12.8 pg/mL) 的比例。

结论

该研究证实了 Sch A 在 AD 中的神经保护作用，表明 Sch A 可能成为一种潜在的抗 AD 药物。