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Cell adhesion molecules play an important role in inflammatory response,angiogenesis and tumor progression. Butein (tetrahydroxychalcone) is a small moleculefrom natural sources, known to be a potential therapeutic drug with anti-inflammatory,anticancer and antioxidant activities. In the present study, we investigated theinhibitory effect of butein on tumor necrosis factor (TNF)-α-induced adhesionmolecule expression and its molecular mechanism of action. Butein significantlydecreased TNF-α-induced monocyte (U937) cell adhesion to lung epithelial cellsin a dose-dependent manner. Butein also inhibited the protein and mRNA expressionof intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesionmolecule-1 (VCAM-1) in TNF-α-stimulated A549 human lung epithelial cells in adose-dependent manner. Butein inhibited TNF-α-induced reactive oxygen species(ROS) generation and nuclear factor-κB (NF-κB) activation in A549 cells; it alsoinhibited the phosphorylation of MAPKs and Akt, suggesting that the MAPK/Akt signalingpathway may be involved in the butein-mediated inhibition of TNF-α-induced leukocyteadhesion to A549 cells. Collectively, our results suggest that butein affectscell adhesion through the inhibition of TNF-α-induced ICAM-1 and VCAM-1 expressionby inhibiting the NF-κB/MAPK/Akt signaling pathway and ROS generation, thereby,elucidating the role of butein in the anti-inflammatory response.

international journal of molecular medicine

Inhibitory effect of butein on tumor necrosis factor-α-induced expression of cell adhesion molecules in human lung epithelial cells via inhibition of reactive oxygen species generation, NF-κB activation and Akt phosphorylation