小胶质细胞
神经炎症
神经保护
化学
MAPK/ERK通路
药理学
肿瘤坏死因子α
中枢神经系统
神经科学
炎症
体内
调节器
前列腺素E
一氧化氮
白细胞介素
信号转导
前列腺素E2
细胞生物学
免疫系统
认知功能衰退
免疫学
整合素αM
阿尔茨海默病
星形胶质细胞
脂多糖
神经胶质
先天免疫系统
作者
Tianqi Huang,Jae Sik Yu,Gyochang Keum,Hyun Ok Yang
标识
DOI:10.1016/j.biopha.2025.118810
摘要
Microglia cells are the initial immune cells regulating neuroinflammation response. Under neuro-degenerative conditions, microglia exhibit as an over-activated phenotype, which generate large amounts of cytokines and inflammatory mediators. Euonymus hamiltonianus Wall. (E. hamiltonianus) showed an effect of enhanced memory and cognitive abilities in Alzheimer Disease (AD) model in our previous research. However, it is remained unknown about the anti-inflammation effect of E. hamiltonianus behind the neurodegenerative situation. The aims of the research are clarifying the possible therapeutic effects and its active compound of E. hamiltonianus on neuro-inflammation on the central nervous system. By the activity guided isolation, dihydrotricetin (compound 1) was identified as an active compound with BV-2 microglia and NMR Spectroscopy. In BV-2 LPS-induced microglial cells, compound 1 inhibited the pro-inflammatory factors, including Prostaglandin E2 (PGE2), interleukin (IL)-6, tumor necrosis factor (TNF)-α, and nitrite oxide (NO) production. This suppressed the activation of microglia in LPS-injected mouse cortex. Besides, the research indicated that compound 1 inhibited PI3K/AKT/IκB/NF-κB and MAPK pathways, and further promoted the inhibition of NLRP3 signaling activation. This research determined that compound 1 is involved in the NRF2/HO-1 signaling and anti-oxidative activity. These data suggest that compound 1 can be a key regulator of microglial activation in LPS-induced neuro-inflammation in vivo and in vitro.
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