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-κ B signaling pathway.
- Author:
Bin-rui YANG
1
;
Nan YU
;
Yan-hui DENG
;
Pui Man HOI
;
Bin YANG
;
Guang-yu LIU
;
Wei-hong CONG
;
Simon Ming-yuen LEE
Author Information
- Publication Type:Journal Article
- MeSH: Berberine Alkaloids; pharmacology; Cell Adhesion; drug effects; Cell Nucleus; drug effects; metabolism; Down-Regulation; drug effects; Human Umbilical Vein Endothelial Cells; cytology; drug effects; metabolism; Humans; Intercellular Adhesion Molecule-1; genetics; metabolism; Monocytes; cytology; drug effects; metabolism; NF-kappa B; metabolism; Protein Transport; drug effects; RNA, Messenger; genetics; metabolism; Signal Transduction; drug effects; Transcription Factor RelA; metabolism; Tumor Necrosis Factor-alpha; pharmacology; Vascular Cell Adhesion Molecule-1; genetics; metabolism
- From: Chinese journal of integrative medicine 2015;21(5):361-368
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate whether I-tetrahydropalmatine (I-THP), an alkaloid mainly present in Corydalis family, could ameliorate early vascular inflammatory responses in atherosclerotic processes.
METHODSFluorescently 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)-κ B in HUVECs.
RESULTSL-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 μ mol/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, I-THP attenuated TNF-α-stimulated NF-κ B nuclear translocation.
CONCLUSIONThese 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 downregulating ICAM-1 and VCAM-1 in vascular endothelial cell based on suppressing NF-κ B.