The natural (poly)phenols as modulators of microglia polarization via TLR4/NF-κB pathway exert anti-inflammatory activity in ischemic stroke.

European Journal of Pharmacology
Ruoqi LiXiang Fan

Abstract

Increasing evidences suggest that inflammation plays a key role in the pathogenesis of stroke, a devastating disease second only to cardiac ischemia as a cause of death worldwide. Microglia are the first non-neuronal cells on the scene during the innate immune response to acute ischemic stroke. Microglia respond to acute brain injury by activating and developing classic M1-like (pro-inflammatory) or alternative M2-like (anti-inflammatory) phenotypes. M1 microglia produce pro-inflammatory cytokines to exacerbate neural death, astrocyte apoptosis, and blood brain barrier (BBB) disruption, while M2 microglia play the opposite role. NF-κB, a central regulator of the inflammatory response, was responsible for microglia M1 and M2 polarization. NF-κB p65 and p50 form a heterodimer to initiate a pro-inflammatory cytokine response, which enhances M1 activation and impair M2 response of microglia. TLR4, expressed on the surface of microglia, plays an important role in activating NF-κB, ultimately causing the M1 response of microglia. Therefore, modulation of microglial phenotypes via TLR4/NF-κB signaling pathway may be a promising therapeutic approach for ischemic stroke. Dietary (poly)phenols are present in various foods, which have sho...Continue Reading

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