Goniothalamin prevents lipopolysaccharide‐induced acute lung injury and inflammation via TLR‐4/NF‐κB signaling pathway

Abstract

AbstractGoniothalamin (GTN) is a natural compound isolated from Goniothalamus species. It is a potent anti‐inflammatory agent. However, there is a paucity of scientific data about its toxicity. This study investigated GTN's anti‐inflammatory mechanism and lipopolysaccharide (LPS)‐induced lung injury in mice. Mice were distributed into four groups and injected with GTN intraperitoneally (Dosage—50 and 100 mg/kg). We analyzed the wet/dry weight ratio, infiltrated inflammatory cell count, myeloperoxidase (MPO) activity, and histopathological changes in the lung tissues of the mice. Results revealed GTN alleviated LPS‐induced inflammation in mice. Western Blot and enzyme‐linked immunosorbent assay techniques were used to investigate the effect of GTN on pro‐inflammatory cytokines and proteins involved in the MAPK and nuclear factor‐B (NF‐κB) signaling pathways. Cytokines (macrophage migration inhibitory factor, interleukin [IL]‐13, IL‐6, TNF‐α, and IL‐1β) were inhibited by GTN. However, IL‐10 was upregulated. Western blot analysis indicated that GTN suppressed the phosphorylation of jun N‐terminal kinase, nuclear factor NF‐kappa‐B p65, I‐kappa‐B, extracellular signal‐regulated kinases, NF‐κB, and p38. GTN also suppressed the expression of TLR‐4 protein, thereby, inhibiting MAPK and NF‐κB signaling pathways. Thus, GTN can effectively prevent and cure acute lung injury.