β-carotene attenuates lipopolysaccharide-induced inflammation via inhibition of the NF-κB, JAK2/STAT3 and JNK/p38 MAPK signaling pathways in macrophages

beta-carotene is one of the most abundant carotenoids, has potential anti-inflammatory effect, it has been reported that beta-carotene could suppress LPS-induced inflammatory responses by inhibiting nuclear factor kappa B (NF-kappa B) translocation, but the more detailed molecular mechanisms underlying the anti-inflammatory action of beta-carotene remain to be fully understood. In this study, we investigated the influence of beta-carotene on the activation of JAK2/STAT3, MAPK, and NF-kappa B signaling pathway induced by LPS in RAW264.7 cells and peritoneal macrophages. Cells were treated with different concentrations of beta-carotene for 3 hr after LPS treatment for 24 hr. The mRNA expression and the release of IL-1 beta, IL-6, and TNF-alpha were evaluated by RT-PCR and ELISA, and the level of signaling proteins of JAK2/STAT3, MAPK, and NF-kappa B signaling pathway were detected by Western blot. The results showed that beta-carotene significantly suppressed (p < 0.05) LPS-induced release of IL-1 beta, IL-6, and TNF-alpha and their mRNA expression. LPS-induced JAK2/STAT3, I kappa B/NF-kappa B p65, JNK/p38 MAPK signal activation were significantly attenuated (p < 0.05) by beta-carotene in a dose-dependent manner. In conclusion, beta-carotene could attenuate LPS-induced inflammation via inhibition of the NF-kappa B, JAK2/STAT3, and JNK/p38 MAPK signaling pathways in macrophages.