Wen Dai

Renmin University of China, Peping, Beijing, China

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Publications (7)14.23 Total impact

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    ABSTRACT: Inflammation is now considered a main pathogenic factor in coronary atherosclerotic heart disease (CHD), and it has a positive correlation with plaque vulnerability. A novel anti-inflammatory factor, milk fat globule-epidermal growth factor 8 (MFG-E8), has been reported as having prominent anti-inflammatory effects in sepsis. However, few studies have reported on the association between MFG-E8 and CHD. In the present study, we aimed to investigate the serum MFG-E8 concentrations in patients with different stages of CHD or without CHD. Then, we studied the associations among MFG-E8, Gensini score, and high-sensitivity C-reactive protein (hs-CRP) in Chinese patients with CHD to illustrate the role of MFG-E8 in CHD. A total of 176 controls and 295 patients with CHD were selected for this study. To evaluate CHD severity, we calculated the Gensini score for all of the subjects. Serum levels of MFG-E8 were determined by an enzyme-linked immunosorbent assay (ELISA) kit; serum total cholesterol (TC), high density lipoprotein-cholesterol (HDL-c), low density lipoprotein-cholesterol (LDL-c), triglyceride (TG), and hs-CRP were detected by an automatic biochemistry analyzer; and fibrinogen (FIB) was analyzed with an automatic coagulation analyzer. Compared with the controls, the CHD group had a lower level of MFG-E8 (673.20 ± 112.34 ng/mL vs. 134.89 ± 4.74 ng/mL, p < 0.001). The level of serum MFG-E8 in the acute myocardial infarction group (118.07 ± 10.10 ng/mL) was significantly less than that in the stable angina group (p = 0.025). Further analysis showed that MFG-E8 had a negative association with the Gensini score and the hs-CRP level (r = -0.590, p < 0.001; r = -0.105, p = 0.022, respectively). In addition, multiple regression analysis of the association between MFG-E8 and the main cardiovascular risk factors in our cases showed that MFG-E8 had a negative association with hs-CRP and a positive association with LDL-c (all p < 0.05). The serum level of MFG-E8 was negatively associated with the severity of coronary artery stenosis and the risk of clinical events. Thus, MFG-E8 has the potential to be a marker of vascular complications.
    Atherosclerosis 01/2014; 233(2):661-665. · 3.71 Impact Factor
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    ABSTRACT: Cardiac myocytes undergo apoptosis under conditions of high free fatty acid concentrations, including palmitate, which is implicated in lipotoxic cardiomyopathy. However, the underlying mechanisms remain unknown. The aim of the present study was to understand the role of reactive oxygen species (ROS) production and the extracellular signal‑regulated kinase 1/2 (ERK1/2) signaling pathway in palmitate‑induced apoptosis in H9c2 cells. H9c2 cells were exposed to palmitate for 12 h. The effect on the cell viability of H9c2 cells was evaluated using the 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide (MTT) assay and cell apoptosis was determined by Hoechst 33342 staining. Levels of intracellular ROS were determined using a peroxide‑sensitive fluorescent probe, 2',7'‑dichlorofluorescein diacetate. Protein expression was measured by western blot analysis. Following treatment with palmitate for 12 h, H9c2 cells apoptosis was demonstrated as increased brightly condensed chromatin or unclear fragments by staining with Hoechst 33342, which was associated with increasing levels of active caspase‑3 and cleaved poly (ADP-ribose) polymerase (PARP). In this model of treatment with palmitate, H9c2 cell apoptosis correlated with increased levels of p53 and Bax expression and reduced levels of Bcl-2 expression. Palmitate‑induced apoptosis was observed to increase levels of intracellular ROS production and p‑ERK1/2 and decrease p‑Akt significantly. Consistent with these results, palmitate‑induced apoptosis was attenuated by the ERK1/2 inhibitor, U0126, through partial reduction of intracellular ROS generation. Collectively, these results indicate that palmitate‑induced apoptosis in H9c2 cells is mediated by activation of the ERK1/2 signaling pathway and increased ROS generation.
    Molecular Medicine Reports 01/2013; · 1.17 Impact Factor
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    ABSTRACT: The association between a common variant of the ESR1 gene rs2234693 and rs9340799 polymorphisms with coronary heart disease (CHD) have been reported, but the available data on this relationship are inconsistent. A meta-analysis was performed to quantitative analysis the association of ESR1 gene polymorphisms and CHD risk using previous case-control studies in Chinese Han population. Several electronic databases were searched for relevant articles up to August 2012. After data collection, a meta-analysis was performed to assess heterogeneity, combine results and evaluate variations. Different effect models were used according to the difference in heterogeneity. Sensitivity analysis was assessed by omitting one study at a time. Publication bias was examined using Begg's funnel plot and Egger's linear regression test. Ten studies covering 3400 subjects on rs2234693 and rs9340799 polymorphisms in the ESR1 gene with CHD risk was included in this meta-analysis. For rs2234693 polymorphism, ten studies were combined to the meta-analysis. A significantly increased CHD risk was found in a dominant model (OR=1.35, 955 CI=1.01-1.81, =0.05), recessive model (OR=1.40, 95% CI=1.15-1.69, =0.0007), and additive model (OR=1.67, 95% CI=1.19-2.34, =0.003). Subgroup for male but not for female showed that the CC genotype could increase the risk of CHD compared with TT and TC genotype in Chinese Han population. Concerning rs9340799 polymorphism, eight studies were combined to the meta-analysis. And no evidence of significant association with CHD risk was found in all genetic models. Our meta-analysis of 10 studies involving Chinese Han population suggests that the CC genotype of the ESR1 rs2234693 polymorphism is significantly associated with an increased risk of CHD in males only. There was no evidence however, of a significant association between the ESR1 rs9340799 polymorphism and CHD risk.
    International journal of medical sciences 01/2013; 10(4):457-66. · 2.07 Impact Factor
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    ABSTRACT: BACKGROUND: Cardiomyocytes apoptosis is an important contributor to myocardial dysfunction and heart failure. Adiponectin has cardioprotective effects, potential mechanisms behind it are not clear in cardiomyocytes. The purpose of the study was to investigate whether adiponectin can block palmitate-induced apoptosis and the underlying biochemical mechanism in H9c2 cells. METHODS: H9c2 cells were treated with palmitate presence or absence of 2.5 mug/mL globular adiponectin. The effect on the cell viability of H9c2 cells was evaluated using MTT assay, and cell apoptosis was determined by Hoechst 33342 staining. Protein expression was measured using the western blot method. RESULTS: Our results showed that the palmitate treatment induced apoptosis in H9c2 cells, which was associated with increasing the level of cleaved caspase-3 and cleaved PARP. Meanwhile, palmitate-induced apoptosis increased the protein level of p-ERK1/2, and decreased the protein level of p-Akt significantly. However, levels of both of these proteins were restored to the normal when pretreated with adiponectin, and followed with the decrease of cleaved caspase-3 and cleaved PARP. In line with these results, the protective effect of adiponectin can be blocked by PI3K/Akt inhibitor LY294002, and palmitate-induced apoptosis can be attenuated by ERK1/2 inhibitor U0126. CONCLUSIONS: Taken together, the present study demonstrated that adiponectin protects H9c2 cells from palmitate-induced apoptosis via PI3K/Akt and ERK1/2 signaling pathways. Our results reveal a link between adiponectin and cardiomyocytes apoptosis, suggesting that adioponectin may be a promising therapeutic for the treatment of lipotoxicity cardiomyopathy.
    Lipids in Health and Disease 10/2012; 11(1):135. · 2.31 Impact Factor
  • Wen Dai, Yan Li, Hongyun Zheng
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    ABSTRACT: Objective: Several groups have reported the important role of the estradiol/testosterone (E(2)/T) ratio in benign prostatic hyperplasia and cerebral vessels. However, there has been no study on the role of the E(2)/T ratio in women with coronary heart disease (CHD). This study aimed to evaluate the association among the ratio of sex hormones and known risk factors of atherosclerosis in postmenopausal women with CHD. Methods: 114 controls and 124 postmenopausal women with CHD were selected for this study. Serum levels of estradiol, testosterone, aromatase, sex hormone-binding globulin (SHBG), lipid-lipoprotein profile and high-sensitivity C-reactive protein were determined. Results: Compared with the control, the E(2)/T ratio decreased from 5.35 ± 2.78 to 3.88 ± 2.51 (p < 0.0001). Multiple linear regression analysis showed that the E(2)/T ratio was negatively associated with total cholesterol, low-density lipoprotein cholesterol (LDL-c) and the atherogenic index of plasma, but positively associated with high-density lipoprotein cholesterol (HDL-c) and HDL-c/LDL-c (for all, p < 0.0001). We found that there was a negative correlation between the E(2)/T ratio and aromatase (r = -0.192, p = 0.032) and a positive correlation between aromatase and SHBG (r = 0.938). Conclusion: The balance of the serum E(2)/T ratio was broken in the women with CHD, and an imbalanced E(2)/T ratio showed a strong association with cardiovascular risk factors in postmenopausal women with CHD.
    Cardiology 05/2012; 121(4):249-254. · 1.52 Impact Factor
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    ABSTRACT: Estrogens protect the vascular system in women, but its effect in men is unclear. We evaluated the impact of estrogen on the male cardiovascular system. Of 140 Chinese males, 55 (aged 61.2 ± 3.5) were cases and 60 (aged 59.5 ± 4.6) were controls. Compared with the control group, only serum estradiol ([E2]; P < .01) levels but not testosterone ([T]; P = .21) were significantly lower in the cases. Linear and multiple regression analysis showed that serum T was positively associated with triglycerides ([TG]; r = .439, P < .01) and d-dimer (r = .258, P < .05) but negatively associated with high-density lipoprotein cholesterol (HDL-C) levels (r = -.267, P < .05) and C-reactive protein (CRP; r = -.214, P < .05). Estradiol was highly associated with TG (r = .783, P < .01) and HDL-C (r = .515, P < .01) but was negatively related with low-density lipoprotein cholesterol (LDL-C; P < .05), total cholesterol/HDL-C (P < .05), CRP (P < .01), and d-dimer (P < .01). In conclusion, serum E2 and T levels affect coronary heart disease risk factors in males.
    Angiology 01/2012; · 2.37 Impact Factor
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    ABSTRACT: Testosterone is either neutral or has a harmful effect on the male cardiovascular system. But the role of imbalance of testosterone (T) and estrogen (E2) (T/E2 ratio) in male CHD has been less studied. This study was carried out with the purpose of evaluating the relationship between T/E2 ratio and CHD. Fifty-five male CHD patients (aged 61.25 ± 3.44) and 60 age-matched controls (aged 59.54 ± 1.44) were selected in this research. Compared with control group, levels of both serum T and E2 decreased, but only E2 had statistical significance (P=0.001). The normal testosterone (T)/estradiol (E2) ratio is 1.7 ± 0.12, but the ratio of T/E2 (3.28 ± 0.58) changed significantly in men with CHD group (P<0.05). With the imbalance of T/E2 ratio in CHD group, we further used a linear and multiple regression methods to analyze the correlation between sex hormones and CHD risk factors. The results showed serum T was positively associated with TG (r=0.439, P<0.01) and D-dimer (r=0.258, P<0.05), but negatively associated with HDL-C (r=-0.267, P<0.05) and Hs-CRP (r=-0.214, P<0.05). However, E2 was highly positive associated with TG (r=0.783, P<0.01) and HDL-C (r=0.515, P<0.01), but was negative related with LDL-C (r=-0.219, P<0.05), TC/LDL (r=-0.236, P<0.05) and D-dimer. Multiple linear regression method also showed the same results between E2 and HDL-C (P=0.020), LDL-C (P=0.000), which showed E2's protective role in cases. However, T/E2's effect is more significative than E2's, and the values between T/E2 and index are HDL-C (r=-0.624, P<0.01), LDL-C (r=0.348, P<0.01), TC/HDL (r=0.237, P<0.05), Hs-CRP (r=0.248, P<0.05) and D-dimer (r=0.249, P<0.05). Multiple linear regression method also showed the positive relationship between T/E2 and HDL-C (P=0.000), D-dimer (P=0.000), and negative relationships between T/E2 and TC (P=0.000), TG (P=0.000) or HDL/LDL (P=0.000). The balance of T/E2 ratio, rather than the absolute levels of androgens, is crucial in modulating the effect of androgens on CHD in males.
    Bio-medical materials and engineering 01/2012; 22(1-3):179-85. · 1.09 Impact Factor