The TIR/BB-loop mimetic AS-1 prevents non-alcoholic steatohepatitis and hepatic insulin resistance by inhibiting NLRP3-ASC inflammasome activation.

ABSTRACT:

Background and purpose

Non-alcoholic steatohepatitis (NASH) is characterized by excessive intracellular lipid accumulation, inflammation and hepatic insulin resistance. As the incidence of NASH is increasing worldwide, there is an urgent need to find novel interventional approaches. The pro-inflammatory cytokine IL-1β, generated and released from Kupffer cells, is considered to initiate the development of NASH. AS-1, a synthetic low-molecule mimetic of myeloid differentiation primary response gene 88 (MyD88), disrupts the interaction between the IL-1 receptor and MyD88. Here, we investigated whether AS-1 could attenuate the pathogenesis of NASH with an emphasis on hepatic insulin resistance.

Experimental approach

Eight-week-old db/db mice were fed a control diet or a methion

SUBMITTER: Wang X 

PROVIDER: S-EPMC5446577 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature