α-Conidendrin inhibits the expression of intercellular adhesion molecule-1 induced by tumor necrosis factor-α in human lung adenocarcinoma A549 cells

• Published in: European journal of pharmacology Vol. 890; p. 173651
• Main Authors: Vo, Nghia Trong, Sasaki, Saki, Miyake, Yasunobu, Nguyen, Nhan Trung, Dang, Phu Hoang, Thi Nguyen, Mai Thanh, Kataoka, Takao
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 05.01.2021
• Subjects: ICAM-1; Lignan; NF-κB; RelA; TNF-α; α-Conidendrin; NF-κB; Lignan; ICAM-1; TNF-α; α-Conidendrin; RelA
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/j.ejphar.2020.173651

α-Conidendrin is a lignan isolated from Taxus wallichiana and other species. In the present study, we demonstrated that α-conidendrin inhibited the cell-surface expression of intercellular adhesion molecule-1 (ICAM-1) induced by tumor necrosis factor-α (TNF-α) at an IC50 value of 40–60 μM in human lung adenocarcinoma A549 cells. α-Conidendrin decreased ICAM-1 protein and mRNA expression levels at concentrations of 40–100 μM in TNF-α-stimulated A549 cells. The TNF-α-induced mRNA expression of vascular cell adhesion molecule-1, E-selectin, and cyclooxygenase-2 was also reduced by α-conidendrin. In the TNF-α-induced nuclear factor κB (NF-κB) signaling pathway, α-conidendrin did not influence the translocation of the NF-κB subunit RelA from the cytoplasm to the nucleus at concentrations up to 100 μM. A chromatin immunoprecipitation assay revealed that α-conidendrin at 100 μM reduced the binding of RelA to the ICAM-1 promoter in response to a stimulation with TNF-α. Collectively, these results indicated that α-conidendrin interfered with the DNA binding of RelA to the ICAM-1 promoter, thereby reducing ICAM-1 transcription. •α-Conidendrin is a lignan isolated from Taxus wallichiana and other species.•α-Conidendrin inhibited TNF-α-induced ICAM-1 expression.•α-Conidendrin did not influence the TNF-α-induced nuclear translocation of RelA.•α-Conidendrin interfered with the DNA binding of RelA to the ICAM-1 promoter.