Curcumin inhibits cigarette smoke-induced inflammation via modulating the PPARγ-NF-κB signaling pathway.

Peroxisome proliferator-activated receptor gamma (PPARγ), a ligand-activated nuclear hormone receptor, is considered to be a potential target for the anti-inflammatory treatment of COPD, and its anti-inflammatory efficacy is likely related to the inhibition of transcriptional regulation of nuclear factor (NF)-κB. Curcumin, a dietary polyphenol isolated from the rhizome of turmeric, has been found to have therapeutic benefits in chronic obstructive pulmonary disease (COPD) via inhibiting NF-κB. However, whether the anti-inflammatory efficacy of curcumin in COPD is associated with PPARγ has scarcely been investigated before. The purpose of this study was to validate the relationship between PPARγ and NF-κB in cigarette smoke (CS)-induced COPD models, and then to investigate whether the therapeutic effect of curcumin on COPD is achieved through modulating the PPARγ-NF-κB signaling pathway. Our experiments in vitro illustrated that PPARγ might be upstream of NF-κB in cigarette smoke extract (CSE)-treated Beas-2B cells, and that curcumin could significantly ameliorate CSE-induced cell viability reduction and inflammation though up-regulating PPARγ and inhibiting NF-κB activation. Importantly, we found that the inhibitory effect on NF-κB by curcumin was dependent on PPARγ in T0070907-treated or PPARγ shRNA-transfected Beas-2B cells, indicating that curcumin inhibited CSE-induced inflammation partially through modulating the PPARγ-NF-κB pathway. Furthermore, we also observed that the effect of curcumin on PPARγ protein expression and NF-κB activation in CS-exposed rats was consistent with the results from experiments in vitro, and curcumin effectively attenuated pulmonary function decline and inflammatory responses in CS-exposed rats. In conclusion, all the results revealed that curcumin attenuated CS-induced inflammation both in vivo and in vitro, presumably by modulating the PPARγ-NF-κB pathway.