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Dihydromyricetin suppresses inflammatory injury in microglial cells to improve neurological behaviors of Alzheimer’s disease mice via the TLR4/MD2 signal

免疫印迹 细胞凋亡 神经炎症 炎症 TLR4型 基因敲除 小胶质细胞 体内 化学 促炎细胞因子 细胞培养 分子生物学 医学 生物 免疫学 生物化学 基因 遗传学 生物技术
作者
Hongyan Pei,Chenyang Han,Jinhao Bi,Zhongmei He,Guo Li
出处
期刊:International Immunopharmacology [Elsevier BV]
卷期号:118: 110037-110037 被引量:15
标识
DOI:10.1016/j.intimp.2023.110037
摘要

We analyzed the role and mechanism of dihydromyricetin (DHM) in suppressing inflammatory injury in microglial cells via targeting MD2.In vitro, BV2 cells were used as the objects of study to induce inflammatory injury with LPS + ATP, then the cell apoptosis level was identified, inflammatory factor levels were measured by ELISA, TLR4 and MD2 were stained with fluorescence staining, and protein expression was determined using Western-blot (WB) assay. Afterwards, MD2 expression was knocked down n BV2 cells to construct the BV2-MD2-/- cell line, so as to detect the role of DHM on BV2-MD2-/-. Moreover, the binding of DHM to MD2 was analyzed via mall molecule-protein docking and pull-down assays. In-vivo, wild-type (WT) C67BL/6 mice and APP/PS1 (AD) mice were used as the objects of study, which were intervened with DHM to detect the changes in mouse cognition. In addition, the pathological changes of brain tissues were analyzed with H&E staining. In addition, the inflammatory factor and protein levels in brain tissues were also detected.DHM suppressed inflammatory injury in BV2 cells, reduced the cell apoptosis rate and inflammatory factor levels, and suppressed the level of TLR4 and MD2. After MD2 knockdown, DHM was unable to further suppress BV2 cell injury. Results of small molecule-protein docking and pull-down assays suggested that DHM bound to MD2 to suppress the formation of TLR4 complex. In AD mice, DHM improved the cognitive disorder in mice, suppressed inflammatory injury in brain tissues and lowered the expression of TLR4 protein.DHM targeted MD2 to suppress the formation of TLR4 protein complex, thereby suppressing inflammatory injury in microglial cells and improving the cognition in AD mice.
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