Publications (11)13.06 Total impact
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Article: Influence of omega-3 polyunsaturated fatty acid-supplementation on platelet aggregation in humans: A meta-analysis of randomized controlled trials.
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ABSTRACT: OBJECTIVE: Increased platelet activity predicts adverse cardiovascular events. The objective was to assess the effects of long-chain omega-3 polyunsaturated fatty acid (n-3 PUFA)-supplementation on platelet aggregation. METHODS AND RESULTS: We conducted a meta-analysis of randomized controlled trials identified using PubMed, Embase and the Cochrane Library. Fifteen studies were included. In comparison to placebo using the random-effect model, n-3 PUFA-supplementation significantly reduced adenosine diphosphate-induced platelet aggregation (standard mean difference [SMD] = -1.23 with 95% confidence interval [CI] -2.24 to -0.23, p = 0.02) and platelet aggregation units, determined using the VerifyNow(®) rapid platelet-function assay system (SMD = -6.78 with 95% CI -12.58 to -0.98, p = 0.02). There was a trend toward decreased collagen-induced (SMD = -0.70 with 95% CI -0.72 to 0.33, p = 0.18) and arachidonic acid-induced platelet aggregation (SMD = -0.43 with 95% CI -2.26 to 1.40, p = 0.64) compared with controls; however, statistical significance was not reached. CONCLUSIONS: Our meta-analysis demonstrates that n-3 PUFA-supplementation is associated with a significant reduction in platelet aggregation when the participants were at poor health status, but not in healthy persons. High-risk patients with cardiovascular disease and even diabetics may potentially benefit from n-3 PUFAs therapy. However, n-3 PUFAs may not be effective in primary prevention. Larger trials need to be carried out to confirm the present findings.Atherosclerosis 11/2012; · 3.79 Impact Factor -
Article: Cardiovascular and cerebrovascular outcomes in elderly hypertensive patients treated with either ARB or ACEI.
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ABSTRACT: Although angiotensin converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) are equally important in the treatment of hypertension, there is less evidence whether they have equal cardiovascular and cerebrovascular protective effects, especially in elder hypertensive patients. This study aims to clarify this unresolved issue. This cross-sectional study included clinical data on 933 aged male patients with hypertension who received either an ARB or ACEI for more than two months between January 2007 and May 2011. The primary outcome was the composite of cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke. The secondary endpoints were unstable angina, new atrial fibrillation, and transient ischemic attack. The median follow-up time was 24 months. Age, drug types, cerebral infarction history, renal dysfunction history were the independent predictors of the primary endpoint. The risk of an occurrence of a primary endpoint event was higher in the ARB group than the ACEI group [P = 0.037, hazard ratios (HR): 2.124, 95% confidence interval (95% CI): 1.048-4.306]. The Kaplan-Meier method also suggests that the rate of primary endpoint occurrence was higher in the ARB group than the ACEI group (P = 0.04). In regard to the secondary endpoints, there were no significant differences between the two treatment arms (P = 0.137, HR: 1.454, 95% CI: 0.888-2.380). Patient age and coronary heart disease history were independent predictors of the secondary endpoint. ACEI were more effective than ARB in reducing cardiovascular and cerebrovascular morbidity and mortality in aged patients with hypertension.Journal of Geriatric Cardiology 09/2012; 9(3):252-7. -
Article: The molecular mechanism of the anticancer effect of atorvastatin: DNA microarray and bioinformatic analyses.
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ABSTRACT: The aim of this study was to identify the molecular mechanisms and biological pathways associated with the anticancer effects of atorvastatin. For this purpose, we conducted cell-based microarray and bioinformatic analyses to determine the effect of atorvastatin exposure on endothelial cell response. The results of bioinformatic analysis performed using the Connectivity Map (cMap) to examine the atorvastatin-induced changes in gene expression in the human umbilical vein endothelial cell line, EA.hy926, indicated that treatment with 10 µM of atorvastatin for 24 h upregulated the expression of 295 genes and downregulated the expression of 354 genes by 2-fold compared to the control treatment. The gene set enrichment analysis (GSEA), the Database for Annotation, Visualization and Integrated Discovery (DAVID) pathway analysis, and Gene Ontology (GO) analysis of differentially expressed genes revealed that Kruppel-like factors (KLFs) and cell cycle-related genes were the genes most significantly affected by atorvastatin treatment. The upregulation of KLFs and the downregulation of the cell cycle-related genes, including cyclin (CCN)A2, CCNE2, CCNB1 and CCNB2, were validated by real-time polymerase chain reaction (RT-PCR). A comparison of the gene expression profile of atorvastatin-treated cells with that of the control cells and with that of 6,100 compounds in the cMap database revealed that the profile of atorvastatin-treated cells was highly similar to that of histone deacetylase (HDAC) inhibitor-treated cells. Therefore, these results suggest that atorvastatin acts as an HDAC, a G1/S (start) and a G2/M (mitosis) cell cycle inhibitor. These findings provide evidence of the feasibility of the use of atorvastatin as an anticancer drug.International Journal of Molecular Medicine 07/2012; · 1.98 Impact Factor -
Article: Irbesartan does not influence the antiplatelet effect of aspirin in spontaneously hypertensive rats.
CNS Neuroscience & Therapeutics 06/2012; 18(8):709-10. · 4.44 Impact Factor -
Article: [Impact of clopidogrel carboxylic metabolite SR26334 on gene expression profile of human umbilical vein endothelial cell line].
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ABSTRACT: This study was purposed to characterize the effect of carboxylic acid metabolite (SR26334) of clopidogrel bisulfate deprived of antiplatelet efficacy on the spectrum of gene expression in the cultured human umbilical vein endothelial cell (HUVEC) line (EA.hy926), and to explore the potential molecule mechanism of SR26334 impact on HUVEC. By using a Affymetrix HU133 plus 2.0 oligonucleotide microarray, the alteration of gene expression spectrum induced by SR26334 in HUVEC was detected, the real-time PCR was used to confirm the results of selected differentially expressing genes. The results indicated that total 235 including 176 up-regulated and 59 down-regulated genes were obtained with change more than 1.5-fold after SR26334 (10 µmol/L) acted on HUVEC for 48 h. SR26334 affected the expression levels of genes involved regulation of transcription, transcription, positive regulation of transcription from RNA polymerase II promoter, cell cycle, cell division, protein amino acid dephosphorylation in HUVEC. It is concluded that carboxylic acid metabolite SR26334 of clopidogrel bisulfate modulates function of endothelial cells through different pathway at gene level.Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 06/2012; 20(3):710-6. -
Article: Protective effects of atorvastatin against oxidized LDL-induced downregulation of KLF expression in EA.hy926 cells.
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ABSTRACT: Krüppel-like transcription factors (KLFs) play a key role in both vascular development and pathophysiological processes, but little is known about the relationship between KLFs and oxidized low-density lipoprotein (ox-LDL). We investigated the effects of ox-LDL on KLF expression. Furthermore, since atorvastatin is commonly used to treat high cholesterol, we also examined the role of this drug in the regulation of KLF expression. The human umbilical vein endothelial cell line EA.hy926 was treated with atorvastatin and ox-LDL alone or in combination, and KLF expression was examined by DNA microarray, semi-quantitative real-time PCR, western blot and immunofluorescence analyses. Atorvastatin upregulated KLF expression in EA.hy926 cells in both the quiescent and ox-LDL-induced inflammatory states, suggesting that KLFs were novel participants in the vascular endothelial dysfunction response to ox-LDL. Our study demonstrated that atorvastatin increased both the mRNA and protein levels of KLF in quiescent EA.hy926 cells. Moreover, atorvastatin counteracted the ox-LDL-induced downregulation of KLF expression.International Journal of Molecular Medicine 05/2012; 30(2):330-6. · 1.98 Impact Factor -
Article: Angiogenesis related gene expression profiles of EA.hy926 cells induced by irbesartan: a possible novel therapeutic approach.
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ABSTRACT: Angiogenesis occurs commonly in various physiological and pathological processes. Improving blood supply through promoting angiogenesis is a novel approach for treating ischemic diseases. Angiotensin II type 1 receptor blockers (ARBs) dominate the management of hypertension, but evidence of their role in angiogenesis is contradictory. Here we explored the angiogenic effects of ARBs through characterizing gene expression of the human umbilical vein endothelial cell line EA.hy926 exposed to irbesartan. The human umbilical vein endothelial cell line EA.hy926 was grown for 72 hours after treatment with different concentrations of irbesartan. The cell proliferative capacity was assessed by CCK8 assay at 24, 48 and 72 hours. Gene expression levels in EA.hy926 cells responding to irbesartan were measured under optimal proliferation conditions by microarray analysis using Affymetrix U133 plus 2.0. The differential expression of genes involved in angiogenesis was identified through cluster analysis of the resulting microarray data. Quantitative RT-PCR and Western blotting analyses were used to validate differential gene expression related to the angiogenesis process. In the 10(-4), 10(-5), 10(-6) mol/L treatment groups, cell proliferation studies revealed significantly increased proliferation in EA.hy926 cells after 24 hours of irbesartan treatment. However, after 48 and 72 hours of treatment with different concentrations of irbesartan, there was no significant difference in cell proliferation observed in any treatment group. We selected the group stimulated with irbersartan at a concentration of 10(-6) mol/L for microarray experiments. Statistical analysis of the microarray data resulted in the identification of 56 gene transcripts whose expression patterns were significantly correlated, negatively or positively, with irbesartan treatment. Cluster analysis showed that these genes were involved in angiogenesis, extracellular stimulus, binding reactions and skeletal system morphogenesis. Of these 56 genes we identified seven genes (VEGF, KDR, PTGS2, PLXND1, ROBO4, LMO2, and COL5A1) involved in the angiogenesis process. qRT-PCR analysis of these genes confirmed the microarray results. Protein expression of three VEGF pathway genes (VEGF, KDR, and PTGS2) was further confirmed by Western blotting. Our study showed that irbesartan may induce angiogenic effects in vascular endothelial cells. It suggested that the mechanism of angiogenic effects of ARBs might be attributed to the signaling cascade from angiotensin receptors in the VEGF pathway. It also provided evidence indicating that ARBs could be used as a novel therapeutic approach to treat chronic ischemic heart disease as well as anti-hypertensive agents.Chinese medical journal 04/2012; 125(8):1369-75. · 0.86 Impact Factor -
Article: [Comparison on the effects of clopidogrel, statins combination in treating coronary artery disease among the elderly patients: a retrospective cohort study].
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ABSTRACT: To compare the effects of clopidogrel with or without combined with CYP3A4-metabolized statin in treating coronary artery disease (CAD) among the elderly patients. The study cohort was defined as all patients were over 60 years of age and hospitalized for CAD who were prescribed clopidogrel between January 2000 and February 2011. A total of 1021 patients were enrolled, with 178 of them prescribed clopidogrel and 843 patients were administrated clopidogrel combined with statins (CYP3A4-metabolized statins 636 and non CYP3A4-metabolized statins 207). The primary endpoint was all cause of death and the second endpoint were non-fatal myocardial infarction (MI), but hospitalized for unstable angina, stroke, transient ischemic attack, or repeated revascularization (PCI or coronary artery bypass graft). Among the clopidogrel group and the clopidogrel plus statins group, the incidence density of death was 6.86/1000 and 3.18/1000 respectively, with crude RR as 2.15 (95%CI: 1.39-3.33) and statistically significant (χ2=3.53, P<0.01). The incidence density of composite thromboembolic events did not show statistical significance (P>0.05). The two groups were 1:1 matched, after propensity score matching, clopidogrel coadministrated with statins group showed significant decrease in all cause of death, with RR as 0.42 (95%CI: 0.19-0.93), χ2=7.23, P<0.01. No significant difference was observed in deaths or composite thromboembolic events between statins via different cytochrome P450 pathways. Clopidogrel with statin could reduce the mortality of elderly CAD patients compared with clopidogrel without statin. The result did not show statistical significance between CYP3A4-metabolized statins or non CYP3A4-metabolized statins regarding the mortality or composite endpoint events.Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi 03/2012; 33(3):337-41. -
Article: [Impact of clopidogrel on gene profile of human umbilical vein endothelial cell line and bioinformatics analysis].
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ABSTRACT: This study was purposed to investigate the effect of clopidogrel on gene expression profile of cultrured human umbilical vein endothelial cell (HUVEC) line (EA.hy926), and explore its potential molecule mechanism. A Affymetrix U133 plus 2.0 oligonucleotide microarray was applied to detect the alteration of gene expression profile induced by clopidogrel in HUVEC. Real time RT-PCR was used to verify the result of selected differentially expressing genes. The results showed that total 508 genes (including 139 up-regulated and 369 down-regulated genes) were obtained with differential expression more than 1.5-fold after clopidogrel (10 µmol/L) acted on HUVEC for 48 h. Clopidogrel affected the expression levels of genes involved protein binding, transcription factor activity, zinc ion binding, regulation of DNA-dependent transcription, transcription, RNA splicing and so on. It is concluded that the clopidogrel modulate function of endothelial cells by regulating sets of genes through different pathway.Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 03/2012; 20(2):466-72. -
Article: [Effect of irbesartan on the proliferation, apoptosis and VEGF mRNA expression of human umbilical vein cell line ea. hy926 in vitro].
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ABSTRACT: To evaluate the effect of irbesartan on the proliferation, apoptosis, and VEGF mRNA expression of human umbilical vein cell line EA.hy926 in vitro. The human umbilical vein cell line EA.hyY926 were treated with various concentrations of irbesartan for 24 h. The cell proliferation after the treatment was detected by CCK8 assay, flow cytometry and FITC Annexin V/PI kit were used to detect changes in the cell apoptosis. RT-PCR was used to evaluate the expression of VEGF mRNA. There were no changes in cell shape with various concentration of irbesartan. CCK-8 assay showed a greater rate of the cell proliferation in irbesartan group than that in control group with a dose-independent manner after 24 h treatment. After incubation with irbesartan, cell proliferation rate was significant (P < 0.05). FCM analysis showed no significantly changes in the cell apoptosis. Irbesartan increased the proliferation of EA.hy926 cells. At concentration of 1 x 10(-4), 1 x 10(-5), 1 x 10(-6) mol/L, VEGF mRNA expression enhanced either (P < 0.05). Irbesartan could promote the proliferation and up-regulated VEGFmRNA expression in EA.hy926 cell line. This result suggested that in addition to antihypertensive effect, angiotensin receptor antagonist might be a novel therapeutic approach to chronic ischemic heart disease as heart failure.Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 01/2012; 28(1):68-71. -
Article: [Irbesartan regulates inflammatory gene expressions related to atherosclerosis in EA.hy926 cells].
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ABSTRACT: To characterize if irbesartan regulates vascular inflammatory gene expression profiles related to atherosclerosis in EA.hy926 cells. Human umbilical vein endothelial cell line EA.hy926 cultured in vitro was incubated with irbesartan (1×10(-6) mol/L) for 24 h. The total RNA was extracted from the cells for gene expression profiling. The DAVID Gene Functional Classification Tool was used to analyze the disease- and function-related genes in the cells. Real-time quantitative polymerase chain reaction (RT-PCR) was used to verify the genes showing differential expression after irbesartan treatment. The protein levels of angiotensin II type 1 receptor (AT1R) and type 2 receptor (AT2R) were tested by Western blotting. Compared with the control cells, 56 genes were found to show marked changes following irbesartan treatment, including 39 up-regulated and 17 down-regulated genes. Disease analysis suggested that these genes were related to such diseases as coronary atherosclerosis, myocardial infarction, and colorectal cancer. Eight genes, namely MMP2, PTGS2, PECAM1, SELP, SELL, CYP1A1, MMRN1, and HSPA1A, were involved in atherosclerosis and myocardial infarction. Verification by RT-PCR produced a result consistent with the gene array result. AT1R was down-regulated while AT2R up-regulated in irbesartan-treated cells. Irbesartan regulates the inflammatory gene expressions related to atherosclerosis in EA.hy926 cells. These inflammatory factors may promote destabilization of atherosclerotic plaque possibly in relation to AT2R overexpression.Nan fang yi ke da xue xue bao = Journal of Southern Medical University 11/2011; 31(11):1835-9.
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2012
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Chinese PLA General Hospital (301 Hospital)
Beijing, Beijing Shi, China -
307 Hospital of the Chinese People's Liberation Army
Beijing, Beijing Shi, China
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