Conclusion
Our results suggest that the anti-inflammatory properties of CIE might result from the inhibition of inflammatory mediators, such as NO, PGE(2), TNF-alpha, and IL-1beta, via suppression of MAPKs and NF-kappaB-dependent pathways.
Methods
Production of NO, PGE(2), TNF-alpha, and IL-1beta by ELISA, mRNA and protein expression of iNOS and COX-2, phosphorylation of MAPKs, and activation of NF-kappaB by RT-PCR and Western blotting were examined in LPS-induced RAW 264.7 macrophages.
Results
The CIE strongly inhibited NO, PGE(2), TNF-alpha, and IL-1beta production, and also significantly inhibited mRNA and protein expression of iNOS and COX-2 in LPS-induced RAW 264.7 macrophages, in a dose-dependent manner. Furthermore, the CIE clearly suppressed nuclear translocation of NF-kappaB p65 subunits, which correlated with an inhibitory effect on IkappaBalpha phosphorylation. The CIE also attenuated the activation of ERK1/2 and JNK in a dose-dependent manner.