It reduces the levels of NO, TNF-α, IL-6, IL-1β and PGs via inhibiting iNOS, NF-κB and COX-2 activity in several in vitro and in vivo LPS-induced inflammation models (148).It reduces oxidative stress, downregulates the TLR4/NF-κB signaling pathway, decreases IL-6 and TNF-α levels, and inhibits mitochondria-mediated neuron apoptosis (195).It acts as potent M1–M2 modulator in adipose tissue macrophages by blocking the inflammatory processes via PPARγ, and it suppresses obesity-related inflammation (196, 197).It inhibits COX-2 and NF-κB gene expression in LPS-mediated acute lung injury (198). This evidence concerns the gene IL1B and acute lung injury.