Tannic acid inhibits NLRP3 inflammasome-mediated IL-1β production via blocking NF-κB signaling in macrophages

The NLRP3 inflammasome rapidly responds to many infections and stress signals and is involved in the pathogenesis of numerous inflammatory disease processes. Tannic acid plays a role in antioxidant, antifungal and antitumor activities. Here, we reported that tannic acid inhibited NLRP3 inflammasome activation by blocking NF-κB signaling to suppress IL-1β secretion. We found that the BMDMs (bone marrow-derived macrophages cells) pre-treated with tannic acid blocked caspase-1 cleavage and inhibited IL-1β secretion in a NLRP3-dependent manner, and suppressed NF-κB signaling activation by inhibiting NF-κB/P65 nuclear localization, suggesting that tannic acid inhibited NLRP3 inflammasome activation. These investigations revealed that tannic acid inhibited NLRP3 inflammasome activation via blocking NF-κB signaling in macrophages, providing us with evidence that tannic acid may be a potent inhibitor for NLRP3-driven diseases. •TA was not cytotoxic but suppressed LPS-induced pro-inflammatory cytokine secretion in BMDMs.•TA inhibited LPS-induced inflammation and inflammatory cytokine production.•TA suppressed NLRP3 inflammasome activation and IL-1β secretion.•TA inhibited NF-κB signaling activation by inhibiting NF-κB/P65 nuclear localization.•Our results showed that tannic acid may be a potent inhibitor for NLRP3-driven diseases.