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Baicalein attenuates acute liver injury by blocking NLRP3 inflammasome.

Abstract：

:Infection and/or drug-mediated acute liver injury, the leading cause of lethal liver failure, is a critical health problem worldwide and lacks effective treatment. Here, we used Lipopolysaccharides (LPS)/D-galactosamine (D-gal)-treated primary hepatocytes to screen a natural library that contains 1130 chemicals. Baicalein in the library showed highest inhibitory effects against LPS/D-Gal-induced liver injury. In-vivo study similarly validated the protection of baicalein against dampened liver function and increased lethality after a challenge of LPS/D-Gal. Using a cytometric bead array, we found that IL-1α and IL-1β, the downstream of NLRP3, had highest reduction among the plasma inflammatory cytokines in LPS/D-Gal-challenged mice after a treatment of baicalein. To determine the target of baicalein and the underlying mechanism, Nlrp3-/-, Gsdmd-/- or WT mice were treated with or without baicalein, IL-1R antibody or recombinant mouse IL-1β (rmIL-1β) prior to a challenge of LPS/D-Gal. Deficiency of Nlrp3 or Gsdmd significantly restored LPS/D-Gal-induced acute liver injury and lethality, and further administration of baicalein did not have additive effects. In addition, the inhibition of the downstream by IL-1R antibody phenocopied the knockout of Nlrp3 or Gsdmd. Moreover, a challenge of rmIL-1β reversed the improvement in Nlrp3-/- mice or the mice treated with baicalein. Taken together, NLRP3 functions as a pivotal promoter in acute liver injury and baicalein attenuates acute liver injury by inhibiting NLRP3 inflammasome.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Xiao T,Cui Y,Ji H,Yan L,Pei D,Qu S

doi

10.1016/j.bbrc.2020.11.109

subject

Has Abstract

pub_date

2021-01-01 00:00:00

pages

212-218

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(20)32153-7

journal_volume

534

pub_type

杂志文章

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