摘要
Objective： TO investigate whether I-tetrahydropalmatine （I-THP）, an alkaloid mainly present in Corydalis family, could ameliorate early vascular inflammatory responses in atheroscleroUc processes. Methods： Fluorescently labeled monocytes were co-incubated with human umbilical vein endothelial cells （HUVECs）, which were pretreated with I-THP and then simulated with tumor necrosis factor （TNF）-α in absence of I-THP to determine if I-THP could reduce thecytokine-induced adhesion of monocytes to HUVECs. Then I-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）- K B 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 proteJn and mRNA expressJon levels of ICAM-1. Furthermore, I-THP attenuated TNF- α -stimulated NF- κ B nuclear translocation. Conclusion： These results provide evidences supporting that I-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- κ B.
Objective： TO investigate whether I-tetrahydropalmatine （I-THP）, an alkaloid mainly present in Corydalis family, could ameliorate early vascular inflammatory responses in atheroscleroUc processes. Methods： Fluorescently labeled monocytes were co-incubated with human umbilical vein endothelial cells （HUVECs）, which were pretreated with I-THP and then simulated with tumor necrosis factor （TNF）-α in absence of I-THP to determine if I-THP could reduce thecytokine-induced adhesion of monocytes to HUVECs. Then I-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）- K B 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 proteJn and mRNA expressJon levels of ICAM-1. Furthermore, I-THP attenuated TNF- α -stimulated NF- κ B nuclear translocation. Conclusion： These results provide evidences supporting that I-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- κ B.
基金
Supported by the grants from the Science and Technology Development Fund,Macao SAR(No.078/2005/A2)
the Science and Technology Plan of Beijing(No.Z141100002214011)
作者简介
Correspondence to： Prof. Simon Ming-Yuen Lee, E-mail： simonlee@ umac.mo; Prof. CONG Wei-hong, E-mail： whongcong79@yahoo. com DOI： 10.1007/sl 1655-015-2165-7
