Neuroprotective effects of natural compounds on LPS-induced inflammatory responses in microglia.

小胶质细胞 神经炎症 神经保护 神经退行性变 药理学 促炎细胞因子 PI3K/AKT/mTOR通路 神经科学 苯丙素 炎症 化学 信号转导 医学 生物 生物化学 免疫学 疾病 病理 生物合成
作者
Jing An,Bin Chen,Xiaoning Kang,Rui Zhang,Yunshan Guo,Jingjing Zhao,Hao Yang
出处
期刊:PubMed 卷期号:12 (6): 2353-2378 被引量:40
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Neuroinflammation is one of the main mechanisms involved in the progression of neurodegeneration. The activation of microglia is the main feature of neuroinflammation, promoting the release of neurotoxic molecules and pro-inflammatory cytokines and resulting in the progressive neuronal cell death. Thus, suppression of the over-activation of microglia using novel pharmacological agents is an attractive issue to alleviate the neuroinflammatory processes associated with neurodegeneration. In recent years, medicinal plants-derived natural compounds have received extensive attention as useful sources of new neuroprotective agents for treating neurological disorders. In this review, we summarized the detailed research progress on the natural compounds derived from medicinal plants with potential anti-inflammatory effects and their molecular mechanisms on modulating the LPS-induced inflammatory responses in microglia. The natural compounds that efficacious in inhibiting the microglia activation include flavonoids, glycosides, phenolics, terpenoids, quinones, alkaloids, lignans, coumarins, chalcone, stilbene and others (biphenyl, phenylpropanoid, oxy carotenoid). They can reduce the expression of neurotoxic mediators (NO, PGE2, iNOS, COX-2) and pro-inflammatory cytokines (IL-6, TNF-α, IL-1β), down-regulate inflammatory markers and prevent neural damage. They exert anti-neuroinflammatory effects by modulating relevant signaling pathways (NF-κB, MAPKs, Nrf2/HO-1, PI3K/Akt, JAK/STAT) as demonstrated by experimental data. The present work reviews the role of microglia activation in neuroinflammation, highlighting the potential anti-inflammatory effects of natural compounds as a promising approach to develop innovative neuroprotective strategy.

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