The expressions of NLRP3, ASC and caspase-1 in KCs of mice liver and in co-culture system and the pro-inflammatory cytokines in the supernatant were reduced significantly in the BMSC-treated group compared to the LPS group.

PGE2 over-expression strengthened the anti-inflammatory ability of BMSCs, but silencing PGE2 reversed this anti-inflammatory effect.

The IL-10 levels in the serum of mice and supernatant of co-culture system were up-regulated by the BMSC treatment. While, ERK1 inhibitor reduced IL-10 production in KCs and blocked the inhibitory effect of PGE2 on the activation of the NLRP3 inflammasome.

Our data reveal a novel mechanism of BMSC-mediated suppression of the activation of KCs through secretion of PGE2 by BMSCs, which promotes KCs to secrete IL-10, leading to the inhibition of the NLRP3 inflammasome in KCs.