Paeoniflorin suppresses the expression of intercellular adhesion molecule-1 (ICAM-1) in endotoxin-treated human monocytic cells
Jin, Lei; Zhang, Li-Min; Xie, Ke-Qiang; Ye, Yang; Feng, Linyin
刊名BRITISH JOURNAL OF PHARMACOLOGY
2011-09
卷号164期号:2B页码:694-703
关键词PF ICAM-1 U937 cell adenosine A(1) receptor NF-kappa B pathway MAPK pathway HUVECs
ISSN号0007-1188
DOI10.1111/j.1476-5381.2011.01464.x
文献子类Article
英文摘要BACKGROUND AND PURPOSE Paeoniflorin (PF) has ameliorative effects on learning and memory impairment and cerebral ischaemia in rats and has protective effects against the degeneration of dopaminergic neurons in substantia nigra. The neuroprotective effects of PF are most probably derived from its anti-inflammatory property. Abnormally high levels of intercellular adhesion molecule-1 (ICAM-1) have been found to be associated with a wide range of inflammatory and immune responses. Here we studied whether PF regulates the levels of ICAM-1 elevated in LPS-activated differentiated human monocytic U937 cells and TNF-alpha-stimulated human umbilical vein endothelial cells (HUVECs). EXPERIMENTAL APPROACH mRNA levels were evaluated by RT-PCR. Protein levels were evaluated by Western blot analysis. An immunofluorescence technique was used to estimate NF-kappa B translocation, and NF-kappa B binding to nuclear DNA was determined by EMSA. KEY RESULTS PF inhibited ICAM-1 expression elevated in LPS-induced U937 cells and TNF-alpha-stimulated HUVECs. Although previous reports showed that PF's action is mediated by activating adenosine A(1) receptors, application of a selective adenosine A(1) receptor antagonist did not change the inhibitory effect of PF in our experiments. To elucidate the underlying mechanisms of the effect of PF, we studied its effect on signalling pathways upstream of ICAM-1 expression. PF suppressed the activation of the NF-kappa B pathway, which regulates the expression of ICAM-1. The TLR4 and MAPK pathways were shown not to be involved in the effects of PF in these cells. CONCLUSIONS AND IMPLICATIONS PF inhibits ICAM-1 expression in LPS-treated U937 cells and TNF-alpha-stimulated HUVECs by suppressing the activation of the NF-kappa B pathway.
资助项目National Basic Research Program of China (973 Program)[2007CB935804] ; National Science Funds Committee[30500612] ; National Science Funds Committee[30570565] ; National Science Funds Committee[C03020706]
WOS关键词NF-KAPPA-B ; HUMAN ENDOTHELIAL-CELLS ; ADENOSINE A(1) RECEPTOR ; SIGNAL-TRANSDUCTION ; EPITHELIAL-CELLS ; UP-REGULATION ; INFLAMMATORY REACTIONS ; GASTRIC-CANCER ; TNF-ALPHA ; IN-VITRO
WOS研究方向Pharmacology & Pharmacy
语种英语
出版者WILEY
WOS记录号WOS:000294367700025
内容类型期刊论文
源URL[http://119.78.100.183/handle/2S10ELR8/278423]  
专题药理学第二研究室
中科院受体结构与功能重点实验室
新药研究国家重点实验室
通讯作者Feng, Linyin
作者单位Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 201203, Peoples R China
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Jin, Lei,Zhang, Li-Min,Xie, Ke-Qiang,et al. Paeoniflorin suppresses the expression of intercellular adhesion molecule-1 (ICAM-1) in endotoxin-treated human monocytic cells[J]. BRITISH JOURNAL OF PHARMACOLOGY,2011,164(2B):694-703.
APA Jin, Lei,Zhang, Li-Min,Xie, Ke-Qiang,Ye, Yang,&Feng, Linyin.(2011).Paeoniflorin suppresses the expression of intercellular adhesion molecule-1 (ICAM-1) in endotoxin-treated human monocytic cells.BRITISH JOURNAL OF PHARMACOLOGY,164(2B),694-703.
MLA Jin, Lei,et al."Paeoniflorin suppresses the expression of intercellular adhesion molecule-1 (ICAM-1) in endotoxin-treated human monocytic cells".BRITISH JOURNAL OF PHARMACOLOGY 164.2B(2011):694-703.
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