Premium
LBE regulates the transformation of Aβ‐activated microglia from M1 state to M2
Author(s) -
Zhongqing Sun,
Chiu Kin
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.047546
Subject(s) - microglia , neuroinflammation , neuroprotection , inflammation , western blot , immunostaining , tumor necrosis factor alpha , blot , chemistry , pharmacology , immunology , biology , biochemistry , immunohistochemistry , gene
Abstract Background Lycium barbarum is a traditional Chinese medicine herb that exhibits a wide variety of biological functions, such as antioxidation, neuroprotection and regulating inflammation. Amyloid‐β‐induced neuroinflammation is one of the key events in the pathogenesis of Alzheimer’s disease with microglia as the main participating cells. Amyloid‐β (Aβ) can activate microglia, change it from the resting state to M1 state, and promote the occurrence of inflammation. This study aims to inversigate the Lycium barbarum extract (LBE) could reverse the active status of microglia activated under Aβ challenge. Method IMG mouse microglial cells were cultured and an LDH assay was performed to determine the toxicity of Aβ and safe dose range of LBE. The ELISA, PCR and Western Blot were used to check the inflammatory factors exposed to Aβ. Immunostaining was used to detect the changes of inflammatory factors, the M1 marker is iNOS, IL‐1β, TNF‐α, and M2 marker is Arg1, Ym1. Result LBE had a dose‐dependent protective effect on IMG cells exposed to o‐Aβ. The ELISA results shew that LBE could decrease the expression of TNF‐α, IL‐6 and IL‐1β inflammatory factors compared with the o‐Aβ alone group in the IMG cell line. The PCR results found that LBE also could inhibit M1‐like inflammatory factors and promote M2 factors in o‐Aβ induced microglia, which is consistent with western blots (WB) results. WB result suggested that LBE suppressed the expression of iNOS, TNF‐α, IL‐6, and IL‐1β and increase the expression of Arg1 compared with the model group. LBE attenuated o‐Aβ‐induced activate microglia by modifying microglia from M1 to M2. Conclusion LBE could modulate the status of activated microglial cells induced by o‐Aβ, and reverse it from M1 to M2 under Aβ treatment.