Open AccessLycium barbarum extract promotes M2 polarization and reduces oligomeric amyloid-β-induced inflammatory reactions in microglial cells
Author(s) -
Zhongqing Sun,
Jinfeng Liu,
Wei Luo,
Ching-Hin Wong,
KwokFai So,
Yong Hu,
Kin Chiu
Publication year - 2022
Publication title -
neural regeneration research/neural regeneration research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.314325
Subject(s) - microglia , tumor necrosis factor alpha , neuroprotection , chemistry , interleukin , nitric oxide synthase , nitric oxide , downregulation and upregulation , inflammation , microbiology and biotechnology , cancer research , pharmacology , cytokine , biochemistry , immunology , medicine , biology , organic chemistry , gene
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.