Xanthium Alleviates LPS-induced Inflammation by Inhibition of JAK/STAT, NF-κB, and MAPK Pathways in Macrophages
Description
Xanthium (Xa) is one of the active ingredients of Xanthium strumarium L. . Here, we focused on exploring the inhibitory effect of Xanthium on inflammation and the potential anti-inflammatory pathways. After LPS-stimulation of the cells, the generation of NO and associated pro-inflammatory factors (TNF-α, IL-1β and IL-6) increased, whereas both were reduced after pretreatment with Xanthium. However, IL-10, an anti-inflammatory factor, was increased by LPS stimulation, which was reduced by Xanthium pretreatment. Furthermore, when compared to LPS-stimulated cells alone, the mRNA expression of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX2), as well as TNF-α, IL-1β and IL-6, was considerably downregulated and suppressed after pretreatment with Xanthium. In addition, Xanthium showed inhibitory effects on iNOS and COX2 at the protein level. Xanthium inhibits both the STAT3 and NF-κB signaling pathways. Xanthium suppresses the inflammatory reaction generated by LPS and exerts anti-inflammatory effects mainly through JAK/STAT, NF-κB and MAPK pathways, among others. Therefore, Xanthium could be a good anti-inflammatory medication candidate.