Open AccessBaicalein Exerts Anti-Neuroinflammatory Effects by Inhibiting the TLR4-ROS /NF-κB-NLRP3 Inflammasome
Author(s) -
Wenyu Xin,
Ming Jing,
Junjie Yang,
Meiling Wang,
GuiGe Hou,
Qiaoyun Wang,
Leiming Zhang,
Chunhua Wang
Publication year - 2021
Publication title -
natural product communications
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.221
H-Index - 44
eISSN - 1934-578X
pISSN - 1555-9475
DOI - 10.1177/1934578x211011385
Subject(s) - baicalein , inflammasome , neuroinflammation , microglia , tlr4 , pharmacology , chemistry , nf κb , inflammation , rotenone , in vivo , caspase 1 , signal transduction , microbiology and biotechnology , receptor , immunology , medicine , biology , biochemistry , mitochondrion
Emerging evidence indicates that NOD-like receptor protein 3 (NLRP3) inflammasome-induced inflammation plays a critical role in the pathogenesis of Parkinson’s disease (PD). Baicalein has been considered as a possible option for PD treatment based on its anti-neuroinflammatory effects. However, no studies have elucidated the precise mechanisms underlying the anti-neuroinflammatory activity of baicalein, particularly inflammasome-mediated effects. In this present study, rotenone-induced PD mice and BV 2 microglia were used to investigate the anti-neuroinflammatory effects of baicalein and explore its underlying mechanism in vivo and in vitro. The results demonstrated that baicalein alleviated motor impairments and attenuated several inflammatory responses in rotenone-induced PD mice. Also, baicalein inhibited the expression of NLRP3 and activated caspase-1 in brain tissues. Correspondingly, baicalein prominently suppressed the inflammatory response in BV 2 microglia induced by rotenone. Furthermore, in vitro data showed that baicalein suppressed the expression of NLRP3 and activated caspase-1 by abrogating the upregulation of ROS, as well as by inhibiting the TLR4/NF-κB signaling cascade. Overall, the results of the present study indicated that baicalein exerted anti-neuroinflammatory effects partly by inhibiting activation of the NLRP3 inflammasome, and targeting NLRP3 inflammasome signaling offers a novel therapeutic strategy for PD treatment.