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-K B Signaling Pathway

• Published in: 中国结合医学杂志：英文版 no. 5; pp. 361 - 368
• Main Author: 杨彬睿 于楠 邓艳辉 许贝文 杨斌 刘光宇 丛伟红 李铭源
• Format: Journal Article
• Language: English
• Published: 2015
• Subjects: 人脐静脉内皮细胞; 信号通路; 单核细胞; 核因子; 细胞黏附分子; 肿瘤坏死因子; 血管内皮细胞; 诱导
• ISSN: 1672-0415; 1993-0402

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.