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| L-Tetrahydropalamatine Inhibits Tumor Necrosis Factor-α-Induced Monocyte-Endothelial Cell Adhesion through Downregulation of Intercellular Adhesion Molecule-1 and Vascular Cell Adhesion Molecule-1 Involving Suppression of Nuclear Factor-κB Signaling Pathway |
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| KeyWord:l-tetrahydropalmatine, atherosclerosis, cell adhesion molecules, tumor necrosis factor-α, nuclear factor-κB |
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| Abstract: |
| Objective: To investigate whether l -tetrahydropalmatine (l -THP), an alkaloid mainly present in Corydalis family, could ameliorate early vascular inflammatory responses in atherosclerotic processes. Methods: Fluorescently labeled monocytes were co-incubated with human umbilical vein endothelial cells (HUVECs), which were pretreated with l-THP and then simulated with tumor necrosis factor (TNF)-α in absence of l-THP to determine if l-THP could reduce thecytokine-induced adhesion of monocytes to HUVECs. Then l-THP were further studied the underlying mechanisms through observing the transcriptional and translational level of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and the nuclear translocation of nuclear factor (NF)-κB in HUVECs. Results: L-THP could block TNF-α-induced adhesion of monocytes to HUVECs and could significantly inhibited the expression of ICAM-1 and VCAM-1 on cell surface by 31% and 36% at 30 μmol/L. L-THP pretreatment could also markedly reduce transcriptional and translational level of VCAM-1 as well as mildly reduce the total protein and mRNA expression levels of ICAM-1. Furthermore, l-THP attenuated TNF-α-stimulated NF-κB nuclear translocation. Conclusion: These results provide evidences supporting that l -THP could be a promising compound in the prevention and treatment of the early vascular inflammatory reaction in atherosclerosis by inhibiting monocyte adhesion to vascular endothelial cell through down-regulating ICAM-1 and VCAM-1 in vascular endothelial cell based on suppressing NF-κB. |
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