中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2022, Vol. 17 ›› Issue (1): 203-209.doi: 10.4103/1673-5374.314325

• 原著:神经损伤修复保护与再生 • 上一篇    下一篇

枸杞提取物促进小胶质细胞M2极化减少寡聚淀粉样β蛋白诱导的炎症反应

  

  • 出版日期:2022-01-05 发布日期:2021-09-22

Lycium barbarum extract promotes M2 polarization and reduces oligomeric amyloid-β-induced inflammatory reactions in microglial cells

Zhong-Qing Sun1, Jin-Feng Liu1, Wei Luo1, Ching-Hin Wong1, Kwok-Fai So1, 2, 3, Yong Hu4, Kin Chiu1, 2, *   

  1. 1Department of Ophthalmology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China; 2State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Hong Kong Special Administrative Region, China; 3Guangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, Guangdong Province, China; 4Department of Orthopaedics & Traumatology, The University of Hong Kong, Hong Kong Special Administrative Region, China
  • Online:2022-01-05 Published:2021-09-22
  • Contact: Kin Chiu, PhD, datwai@hku.hk.
  • Supported by:
    This work was supported by Midstream Research Program for Universities, Hong Kong Special Administrative Region, China, No. MRP-092-17X. 

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摘要：

枸杞是一种传统中药，具有抗氧化、神经保护和免疫调节等多种生物学功能。阿尔茨海默病发病的主要机制之一是被淀粉样β蛋白激活的小胶质细胞从静止态转化为M1态，并向其周围释放促炎性细胞因子。为观察枸杞提取物体外对寡聚淀粉样β蛋白诱导的活化小胶质细胞的作用，实验将经枸杞提取物预处理1h的永生化小胶质细胞以寡聚淀粉样β蛋白诱导干预23h。见枸杞提取物可明显增加寡聚淀粉样β蛋白诱导小胶质细胞的存活率，抑制M1促炎标记物诱导性一氧化氮合酶、肿瘤坏死因子α、白细胞介素6和白细胞介素1β的表达水平，上调M2抗炎标记物精氨酸酶1的免疫阳性表达以及精氨酸酶1、Ym1、白细胞介素4的表达水平。枸杞提取物还抑制了寡聚淀粉样β蛋白诱导细胞中肿瘤坏死因子α、白细胞介素6和白细胞介素1β的分泌。体外细胞学实验证明了枸杞提取物可抑制寡聚淀粉样β蛋白诱导小胶质细胞M1极化以及其伴随的炎症反应，并趋向于促进M2极化的发生。

https://orcid.org/0000-0001-6581-9007 (Chiu Kin)

关键词: 枸杞提取物, Aβ, M1小胶质细胞, M2小胶质细胞, 促炎因子, 抗炎因子, 神经炎症, 阿尔茨海默病

Abstract: Lycium barbarum (LB) is a traditional Chinese medicine that has been demonstrated to exhibit a wide variety of biological functions, such as antioxidation, neuroprotection, and immune modulation. One of the main mechanisms of Alzheimer’s disease is that microglia activated by amyloid beta (Aβ) transform from the resting state to an M1 state and release pro-inflammatory cytokines to the surrounding environment. In the present study, immortalized microglial cells were pretreated with L. barbarum extract for 1 hour and then treated with oligomeric Aβ for 23 hours. The results showed that LB extract significantly increased the survival of oligomeric Aβ-induced microglial cells, downregulated the expression of M1 pro-inflammatory markers (inducible nitric oxide synthase, tumor necrosis factor α, interleukin-6, and interleukin-1β), and upregulated the expression of M2 anti-inflammatory markers (arginase-1, chitinase-like protein 3, and interleukin-4). LB extract also inhibited the oligomeric Aβ-induced secretion of tumor necrosis factor α, interleukin-6, and interleukin-1β in microglial cells. The results of in vitro cytological experiments suggest that, in microglial cells, LB extract can inhibit oligomeric Aβ-induced M1 polarization and concomitant inflammatory reactions, and promote M2 polarization.

Key words: Alzheimer’s disease, amyloid-β, anti-inflammatory factors, Lycium barbarum extract, M1 microglia, M2 microglia, neuroinflammation, proinflammatory factors