Tannic acid inhibits NLRP3 inflammasome-mediated IL-1β production via blocking NF-κB signaling in macrophages
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, 361102 (China)
- Respiratory Medicine, Second Affiliated Hospital of Xiamen Medical College, Xiamen, Fujian, 361000 (China)
- Blood Transfusion Department, Zhongshan Hospital of Xiamen University, Xiamen, Fujian, 361004 (China)
- Department of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, Xiamen, Fujian, 361004 (China)
Highlights: • 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. 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.
- OSTI ID:
- 23134257
- Journal Information:
- Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 4 Vol. 503; ISSN 0006-291X; ISSN BBRCA9
- Country of Publication:
- United States
- Language:
- English
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