Pinocembrin relieves lipopolysaccharide and bleomycin induced lung inflammation via inhibiting TLR4-NF-κB-NLRP3 inflammasome signaling pathway.

Int Immunopharmacol

State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin 300353, China; Tianjin Key Laboratory of Molecular Drug Research, Tianjin International Joint Academy of Biomedicine, Tianjin 300457, China; Tianjin Key Laboratory of Early Druggability Evaluation of Innovative Drugs, Tianjin 300457, China. Electronic address:

Published: January 2021

Inflammation is a defense response of the body to stimuli. Lung injury caused by external stimuli can stimulate inflammatory cells to accumulate at the site of injury and secrete cytokines. Pinocembrin is a flavonoid with anti-inflammatory effects. Based on previous studies, we further explored the anti-inflammatory mechanisms of pinocembrin in vitro and in vivo. In vitro studies indicated that pinocembrin inhibited lipopolysaccharide (LPS)-stimulated inflammatory response in macrophages. In vivo studies also showed that pinocembrin could reduce LPS and bleomycin (BLM) induced lung inflammatory response in mice. Further mechanistic studies indicated that pinocembrin could regulate the TLR4-NF-κB signaling pathway and suppressed the activation and assembly of NLRP3 inflammasomes. In summary, pinocembrin could relieve pulmonary inflammatory response induced by LPS and BLM mainly via inhibiting TLR4-NF-κB-NLRP3 inflammasome axis. These results contribute to the understanding of the anti-inflammatory mechanisms of pinocembrin and serve as reference for future research on pinocembrin.

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http://dx.doi.org/10.1016/j.intimp.2020.107230DOI Listing

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