Abstract:
:Thalidomide is an antiangiogenic drug and is clinically useful in a number of cancers. However, the molecular mechanism by which thalidomide exerts its antitumor effects is poorly understood. This study was designed to clarify the relationship between antiangiogenesis and antitumor effects of thalidomide and to explore the molecular mechanism for its antitumor activity. We evaluated the effects of thalidomide on the growth of human tumor cells expressing (MCF-7 and HL-60) or not expressing (HeLa and K562) COX-2 in vitro. We also studied the effects of thalidomide on COX-1, COX-2 or bcl-2 expression, TNFalpha, VEGF, GSH and cytochrome c in these cells. Thalidomide could inhibit tumor growth in a concentration-dependent manner in MCF-7 and HL-60; its IC50s for them were 18.36+/-2.34 and 22.14+/-2.15 microM, respectively, while this effect was not observed in HeLa and K562. Thalidomide reduced COX-2 expression accompanied by a decrease of bcl-2 protein, TNFalpha, VEGF, GSH and an increased cytochrome c, but had no effect on that of COX-1, in MCF-7 and HL-60. Moreover, cells not expressing COX-2 were insensitive to the growth-inhibitory and effects on cytokines of thalidomide. In our mouse xenograft model of OVCAR-3 and HCT-8, we found that thalidomide could decrease intratumoral microvessel density in both tumors; it exerted antitumor effects only on OVCAR-3 expressing COX-2 but did not on HCT-8 not expressing COX-2. Effect of thalidomide on COX-1 and COX-2 in vivo was consistent with that of in vitro. These results demonstrated that thalidomide might inhibit growth of tumors through COX-2 degradation independent of antiangiogenesis.
journal_name
Vascul Pharmacoljournal_title
Vascular pharmacologyauthors
Du GJ,Lin HH,Xu QT,Wang MWdoi
10.1016/j.vph.2005.04.003keywords:
subject
Has Abstractpub_date
2005-08-01 00:00:00pages
112-9issue
2eissn
1537-1891issn
1879-3649pii
S1537-1891(05)00101-1journal_volume
43pub_type
杂志文章abstract:BACKGROUND:Proprotein convertase subtilisin-kexin type 9 inhibitors (PCSK9-I) reduce low-density lipoprotein (LDL) cholesterol in human studies. Previous studies suggest that PCSK9-I may also affect very-low-density lipoproteins (VLDL). We therefore studied VLDL size and composition in a "real-world" study population w...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2019.03.002
更新日期:2019-05-01 00:00:00
abstract::Stem cells possess the ability of self-renewal and give rise to specific cell types. The differentiation of stem cells involves environmental factors, transduction of extra and intra-cellular signals, regulation of gene expression by transcriptional factors, microRNAs and chromosome structural modifiers. Vascular SMCs...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2012.02.014
更新日期:2012-05-01 00:00:00
abstract::An endothelial dysfunction generates a proatherogenic environment characterized by stimulating thrombus formation. Epidemiological studies have provided evidence of a protective role of healthy diets in the prevention of cardiovascular diseases. Hydroxycinnamic acids constitute abundant polyphenols in our diets as the...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2014.10.006
更新日期:2014-12-01 00:00:00
abstract::Arterial hypertension is a condition associated with endothelial dysfunction, accompanied by an imbalance in the production of reactive oxygen species (ROS) and NO. The aim of this study was to investigate and elucidate the possible mechanisms of sildenafil, a selective phosphodiesterase-5 inhibitor, actions on endoth...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2019.106601
更新日期:2020-01-01 00:00:00
abstract::Norepinephrine (NE) responses are larger in renal and femoral veins compared to phenylephrine (PE). These differences may be due to the subtypes of adrenoceptor involved in these responses or to the involvement of local modulatory mechanisms. Therefore, the present study investigated in organ bath the adrenoceptor sub...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2015.06.017
更新日期:2015-09-01 00:00:00
abstract::The objective of this study was to determine the mechanism by which Na(+)/H(+) exchanger (NHE) inhibitors induce vasodilatation. The NHE inhibitors, 5-(N,N-dimethyl)-amiloride (DMA), cariporide, and amiloride, evoked endothelium-dependent relaxation in rat aortas with ED50 values of 16, 89, and 148μM, respectively, an...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2012.11.004
更新日期:2013-04-01 00:00:00
abstract:BACKGROUND:Antitumor activity of paclitaxel is based on promotion of abnormal microtubule (MT) assembly but it is also considered to have significant pro-inflammatory and anti-angiogenic effects in vivo and thus may cause vascular dysfunction. METHODS:We studied 27 women treated with paclitaxel-containing combinations...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2010.05.002
更新日期:2010-09-01 00:00:00
abstract:BACKGROUND:Platelets play crucial roles in the development of arterial thrombosis and other pathophysiologies leading to clinical ischemic events. Defective regulation of platelet activation/aggregation is a predominant cause for arterial thrombosis. The purposes of the study are to determine whether atherosclerotic pl...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2008.03.004
更新日期:2008-07-01 00:00:00
abstract::Venous and arterial walls are responsive to sympathetic system and circulating substances, nevertheless, very few is known about the venous blood flow regulation simultaneously to arterial vascular beds. In this study, we compared the venous and arterial blood flow regulation in visceral and muscular beds upon injecti...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2017.09.007
更新日期:2017-12-01 00:00:00
abstract::Prostaglandin E2 (PGE2), a cyclooxygenase metabolite that generally acts as a systemic vasodepressor, has been shown to have vasopressor effects under certain physiologic conditions. Previous studies have demonstrated that PGE2 receptor signaling modulates angiotensin II (Ang II)-induced hypertension, but the interact...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.05.015
更新日期:2016-09-01 00:00:00
abstract::Autoimmune rheumatic diseases are characterised by systemic inflammation and complex immunopathology, with an increased risk of cardiovascular disease, initiated by endothelial dysfunction in a chronic inflammatory environment. Endothelial microparticles (EMPs) are released into the circulation from activated endothel...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2016.05.016
更新日期:2016-11-01 00:00:00
abstract::Hyperhomocysteinemia (HHcy) is a metabolic disorder marked by an excess amount of the amino acid homocysteine (Hcy) in the blood stream. Hcy is a H(2)S precursor-formed from the metabolism of methionine. Elevated Hcy levels have been associated with higher blood pressure. However, the precise contribution of H(2)S to ...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2010.05.004
更新日期:2010-09-01 00:00:00
abstract::Propionyl-l-carnitine (PLC) is a natural short-chain derivative of l-carnitine (LC), a natural amino acid that plays an important role in fatty acid metabolism. Recent studies suggest that PLC has vascular protective effects. Because of the importance of endothelial nitric oxide synthase (eNOS) and its product, antiat...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2013.07.001
更新日期:2013-09-01 00:00:00
abstract::Excessive iron can generate reactive oxygen species (ROS), leading to oxidative stress that is closely associated with cardiovascular dysfunction. Iron overload was induced in male ICR mice by injection of iron sucrose (10mg/kg/day) for eight weeks. Iron overload was evidenced by increased serum iron indices. The mice...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.10.001
更新日期:2016-12-01 00:00:00
abstract::Results of our previous studies have suggested that enhanced generation of superoxide (O2(-)) may contribute to the pathophysiology of hypertension in Ren-2 transgenic rats (TGR). The present study was performed to evaluate in TGR the effects of chronic treatment with the O2(-) scavenger tempol and the antioxidant apo...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2009.06.001
更新日期:2009-08-01 00:00:00
abstract::Nitric oxide (NO) donors are commonly used for the prevention and treatment of ischemic heart disease. Besides their effects on the heart, NO donors may also prevent hypoxic brain damage and exert beneficial effects on atherosclerosis by favoring features of plaque stability. We recently described that apolipoprotein ...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2019.05.001
更新日期:2019-01-01 00:00:00
abstract:BACKGROUND:Macrophages play a central role in atherosclerosis development and progression, hence, targeting macrophage activity is considered an attractive therapeutic. Recently, we documented nanomedicinal delivery of the anti-inflammatory compound prednisolone to atherosclerotic plaque macrophages in patients, which ...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.04.006
更新日期:2016-07-01 00:00:00
abstract::Recent evidence showed that 17 β-estradiol (E₂) decreased cytokine-induced expression of cell adhesion molecules (CAM). Changes in intracellular Ca²+ concentration ([Ca²+](i)) has been shown to be associated with CAM expression in endothelial cells. Here, the effects of E₂ (1 μM, 24 h) on the expression of intracellul...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2010.09.001
更新日期:2010-11-01 00:00:00
abstract::We studied the mechanisms involved in the relaxation induced by nitric oxide (NO) donors, ruthenium complex ([Ru(terpy)(bdq)NO(+)](3+)-TERPY) and sodium nitroprusside (SNP) in denuded rat aorta. Both NO donors induced vascular relaxation independent of the agonist used in the pre-contraction. [Ru(terpy)(bdq)NO(+)](3+)...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2006.10.002
更新日期:2007-03-01 00:00:00
abstract::β-Adrenoceptors (β-ARs) modulate ERK1/2 and p38 in different cells, but little is known about the contribution of these signaling pathways to the function of β-ARs in vascular tissue. Immunoblotting analysis of rat aortic rings, primary endothelial (ECs) and smooth muscle cells (SMCs) isolated from aorta showed that β...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2014.04.003
更新日期:2014-05-01 00:00:00
abstract::Upon myocardial infarction (MI) immune system becomes activated by extensive necrosis of cardiomyocytes releasing intracellular molecules called damage-associated molecular patterns. Overactive and prolonged immune responses are likely to be responsible for heart failure development and progression in patients survivi...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2018.08.011
更新日期:2019-01-01 00:00:00
abstract:OBJECTIVE:In patients with familial combined hyperlipidemia (FCHL), without metabolic syndrome (MS), occurrence of non-alcoholic fatty liver disease (NAFLD) is related to a specific pro-inflammatory profile, influenced by genetic traits, involved in oxidative stress and adipokine secretion. Among FCHL or MS patients, h...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2015.04.004
更新日期:2015-09-01 00:00:00
abstract::The purpose of this study was to determine if P-selectin, an adhesion molecule involved in the transendothelial movement of leukocytes, might also have a direct influence on the function of cells that come into contact with it. Human peripheral blood mononuclear cells were incubated on immobilized P-selectin or a cont...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2005.11.002
更新日期:2006-03-01 00:00:00
abstract::Systemic inflammatory response syndrome (SIRS), initially reported after cardiovascular surgery, has been described after various interventional cardiology procedures, including endovascular/thoracic aortic repair (EVAR/TEVAR), implantation of heart rhythm devices, percutaneous coronary intervention (PCI), electrophys...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2018.04.003
更新日期:2018-04-12 00:00:00
abstract:AIM:Local levels of angiotensin peptides depend on their rates of production and degradation, which induce proatherogenic or atheroprotective effects. Here, we reveal the kinetics of Angiotensin-I metabolism in paired early and advanced atherosclerotic lesions. METHODS:Lesions were spiked with labeled Ang-I* and super...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.08.001
更新日期:2016-10-01 00:00:00
abstract::There is little information about the direct effect of caffeine in human blood vessels. The purpose of this study was to evaluate the direct vascular effect of caffeine on human internal mammary artery (IMA) and the involvement of potassium channels in this response. Segments of IMA were obtained from 29 patients who ...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2008.11.002
更新日期:2009-03-01 00:00:00
abstract::Elevated plasma levels of factor VII and fibrinogen are risk factors for cardiovascular disease, especially arterial thrombosis. Oral contraceptive use increases factor VII and fibrinogen plasma levels. It has been described that DNA polymorphisms are associated with the plasma levels of hemostatic variables and their...
journal_title:Vascular pharmacology
pub_type: 临床试验,杂志文章,随机对照试验
doi:10.1016/s1537-1891(02)00300-2
更新日期:2002-08-01 00:00:00
abstract::A small amount of adipose tissue associated with small arteries and arterioles is encountered both in mice and man. This perivascular adipose tissue (PVAT) has a paracrine effect on the vascular tone regulation. PVAT is expanded in obesity and in diabetes. This expansion not only involves enlargement of fat cells, but...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2012.02.003
更新日期:2012-05-01 00:00:00
abstract::In systemic sclerosis, microvascular injury often precedes the development of fibrosis. Whereas the development of digital ulcers and skin fibrosis causes high morbidity, the affection of internal organs, in particular complications such as interstitial lung disease and pulmonary (arterial) hypertension, account for t...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2012.12.001
更新日期:2013-03-01 00:00:00
abstract::Unresolved endoplasmic reticulum (ER) stress, with the subsequent persistent activation of the unfolded protein response (UPR) is a well-recognized mechanism of endothelial cell apoptosis with a major impact on the integrity of the endothelium during the course of cardiovascular diseases. As in other cell types, Ca(2+...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2015.07.011
更新日期:2016-01-01 00:00:00