Cianidanol from Sea Buckthorn Exert Anti-Inflammatory Effects by the Inhibiting JAK2/STAT3 Signaling Pathway via an Integrative Pharmacology Strategy.

Abstract

Sea buckthorn is a model of medicine and food homology, but the chemical composition and mechanism of anti-inflammatory effects are limited. In this study, the key components and mechanisms of the anti-inflammatory effects of sea buckthorn were identified based on UPLC-Q-TOF-MS, network pharmacology, molecular docking, molecular dynamics and RAW264.7 cells. The predicted key anti-inflammatory compounds in sea buckthorns were cianidanol, kaempferol, pelargonidin, and ent-epicatechin, and the key targets were EGFR, TNF, STAT3, and IL-10. The anti-inflammatory effects of sea buckthorn may be achieved via the synergistic regulation of multiple biological pathways. Furthermore, cianidanol significantly reduced the secretion of NO, IL-6, TNF-α, and IL-1β and the expression of phosphorylated JAK2 and STAT3 in LPS-stimulated RAW264.7 cells, as determined by ELISA and western blotting. Cianidanol from sea buckthorns exerts anti-inflammatory effects by reducing the expression of inflammatory mediators and pro-inflammatory cytokines, and inhibiting the JAK2/STAT3 signaling pathway. Thus, sea buckthorn can be developed into a promising functional food with anti-inflammatory properties.