Search

Background: High glucose could induce structure and function change in cardiomyocytes, PKC plays a core effect in the onset and progression of diabetic cardiomyopathy, but its underlying downstream signal transduction pathway is still not completely understood. Objectives: To study the influence of high glucose on the structure, function and signal transduction pathway of PKC (Protein Kinase C)/NF-κB(Nuclear factor-κB)/c-fos in cultured cardiomyocytes. Methods: Using cultured cardiomyocytes of neonatal Sprague-Dawley rats as a model, groups were divided into: control group (glucose: 5 mmol/L); high glucose group (glucose: 10 mmol/L, 15 mmol/L, 20 mmol/L, 25.5 mmol/L); equimolar mannital group (5 mmol/L glucose + 20.5 mmol/L maninital); high glucose(25.5 mmol/L) add PKC inhibitor (Ro-31-8220, 50 nmol/L); high glucose (25.5 mmol/L) add NF-κB inhibitor (BAY11-7082, 5 μmol/L). The cellular contracting frequency and volumes were measured and the expression of PKC-α, PKC-β2, p-PKC-α, p-PKC-β2, NF-κB, p-NF-κB, TNF-α (tumor necrosis factor-α) and c-fos were measured by western blot or RT-PCR. Results: Cardiomyocytes cultured in high glucose level, but not iso-osmotic mannital, showed an increased pulsatile frequency and higher cellular volumes consistent with the increased glucose levels, and also higher expression of PKC-α, PKC-β2, p-PKC-α, p-PKC-β2, NF-κB, p-NF-κB, TNF-α and c-fos. The addition of Ro-31-8220 and BAY11-7082 could partly reverse these changes induced by high glucose level. Conclusion: High glucose significantly increased the pulsatile frequency and cellular volumes of cultured cardiomyocytes via PKC/NF-κB/c-fos pathway, which might lead to diabetic cardiomyopathy. [ABSTRACT FROM AUTHOR]

Aims: The aim of this study is to investigate whether angiotensin-converting enzyme inhibitor (ACEI) therapy with ramipril could augment circulating endothelial progenitor cells (EPCs) with enhanced functional activity in patients with stable coronary artery diseases.Methods and results: 20 patients with angiographically documented stable coronary artery disease (CAD) were prospectively treated with 5 mg of ramipril per day for 4 weeks. Before and weekly after the initiation of ramipril therapy, EPCs were isolated from peripheral blood and counted. Ramipril treatment of patients with stable CAD was associated with an approximately 1.5-fold increase in the number of circulating EPCs by 1 week after initiation of treatment; this was followed by sustained increased levels to approximately 2.5-fold throughout the 4-week study period. In addition, ramipril treatmen was associated with increases in the functional activity of EPCs, as assessed by their proliferation, migration, adhesion and in vitro vasculogenesis capacity.Conclusion: The results of the present study define a novel mechanism of action of ACEI treatment in patients with stable CAD: the augmentation of circulating EPCs with enhanced functional activity. Given the well-established role of EPCs of participating in repair after ischemic injury, stimulation of EPCs by ACEI may contribute to the clinical benefit of ACEI therapy in patients with CAD. [ABSTRACT FROM AUTHOR]

Brucellosis and Toxoplasmosis are important zoonotic diseases, and Neospora caninum is a parasite causing disease in cattle and other animals. Brucella spp. and N. caninum can cause abortions in cattle, and Toxoplasmosis is a relevant cause of abortion for small ruminants, resulting in economic loses to farmers. In this study, from July 2015 to April 2017, a total of 535 Yanbian yellow cattle blood samples were collected from 3 cities in Jilin Province, China. We detected the frequency of N. caninum, Toxoplasma gondii, and Brucella spp. using enzyme-linked immunosorbent assays, indirect hemagglutination assay, and real-time PCR methods, respectively. The frequency of Brucella was 7.7% (41/535), and the seroprevalences of N. caninum and T. gondii were 6.2% (33/535) and 5.0% (27/535), respectively. The region, gender, and age of Yanbian yellow cattle were considered as risk factors when analyzed using a logistic regression model. These findings provide the foundation for the prevention and control of infection by these pathogens in Yanbian yellow cattle and humans.

Objective: To determine the effect of proton pump inhibitor (PPI) on in-stent restenosis (ISR) in patients receiving clopidogrel therapy., Methods: Total 439 patients underwent percutaneous coronary intervention (PCI) were enrolled in the study,including 250 post-PCI patients discharged on clopidogrel alone and 189 patients discharged on clopidogrel with PPI. The in-stent restenosis (ISR) ratio of the patients in these two groups were observed., Results: During a mean follow-up period of (13 ± 5.9) months, the post-PCI patients discharged on concomitant clopidogrel-PPI therapy had higher risk of ISR than those discharged on clopidogrel alone (19.6% Compared with 8%, P<0.001)., Conclusion: Concomitant use of clopidogrel and PPI after hospital discharge would increase the risk of ISR for post-PCI patients.

The purpose of this study is to investigate the effect of chelerythrine on the hypertrophy of cardiomyocytes of neonatal rats induced by different glucose levels and its mechanism. Using cultured neonatal ventricular myocytes as a model, groups were divided as: control (5 mmol x L(-1)); high glucose level (10, 15, 20, and 25.5 mmol x L(-1)); high glucose level (25.5 mmol x L(-1)) add different concentrations of chelerythrine (1 and 8 micromol x L(-1)); and control glucose level (5 mmol x L(-1)) add different concentrations of chelerythrine (1 and 8 micromol x L(-1)). Different groups of cardiomyocytes after adding corresponding treat factors were cultured for 48 hours. Cardiomyocytes' diameters and protein level were measured and the expression of PKC-alpha, PKC-beta2, p-PKC-alpha, and p-PKC-beta2 were measured by Western blotting. Compared with control group, neonatal myocytes cultured in high glucose levels showed increased cellular volumes, protein level and expression of PKC-alpha, PKC-beta2, p-PKC-alpha, p-PKC-beta2. When chelerythrine was added, cellular volumes, protein level and expression of PKC-alpha, PKC-beta2, p-PKC-alpha, p-PKC-beta2 were significantly reduced. But in 1 micromol x L(-1) chelerythrine group, the expression of PKC-beta2 was not significantly reduced. The result suggested that chelerythrine can reverse the hypertrophy induced by different glucose levels on the cardiac myocytes, it may have protective effect against diabetic cardiomyopathy via PKC passageway.

Objective: To investigate alterations of endothelial progenitor cells (EPCs) from peripheral blood in patients with coronary heart diseases., Methods: Twenty patients with coronary heart diseases (CHD) and 20 matched control subjects were included in the study. Total mononuclear cells (MNCs) were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. After cultured for 7 days, attached cells were cytochemically analyzed. EPCs were characterized as adherent cells double positive for DiLDL-uptake and lectin-binding by laser scanning confocal microscope with direct fluorescent staining. EPCs proliferation and migration were measured by MTT assay and modified Boyden chamber assay, respectively. EPCs adhesion assay was performed by replating on fibronectin-coated dishes, then adherent cells were counted., Results: The number of EPCs was significantly reduced in patients with CHD compared with that of age-matched control subjects (31.8+/-7.7 compared with 59.5 +/-10.6 EPCs/x 200 field; P<0.05). In addition, the functional activity of EPCs such as proliferation, migration and adhesive capacity was also impaired in patients with CHD., Conclusion: EPCs number and functional activity are significantly decreased in patients with CHD.

Aim: To investigate whether Ginkgo biloba extract can augment endothelial progenitor cell (EPC) number, and promote EPC proliferation, migration and adhesion., Methods: Total mononuclear cells (MNCs) were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. After 7 days of culture, attached cells were stimulated with Ginkgo biloba extract (10, 25 and 50 mg x L(-1)) or vehicle control for the respective time points (6, 12, 24 and 48 h). EPC were characterized as adherent cells double positive for DiLDL-uptake and lectin binding by direct fluorescent staining under a laser scanning confocal microscope. EPC were further documented by demonstrating the expression of CD34, VEGFR-2 and AC133 with flow cytometry. EPC proliferation, migration and in vitro vasculogenesis activity were assayed with MTT assay, modified Boyden chamber assay and in vitro vasculogenesis kit, respectively. EPCs adhesion assay was performed by replating MNCs on fibronectin-coated dishes, and then counting adherent cells., Results: Incubation of isolated human MNCs with Ginkgo biloba extract increased the number of EPC, maximum at 25 mg x L(-1), 24 hours (approximately 1-fold increase, P < 0.01). In addition, Ginkgo biloba extract promotes EPC proliferative, migratory, adhesive and in vitro vasculogenesis capacity., Conclusion: Ginkgo biloba may promote EPC augmentation and enhance its functional activity.

Objective: To investigate whether puerarin can augment endothelial progenitor cells (EPCs) numbers, promote EPC proliferation, migration and adhesion., Method: Total mononuclear cells (MNCs) were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. After 7 days culture, attached cells were stimulated with puerarin (to make a series of final concentrations: 0. 1, 0.5, 1, 3 mmol x L(-1)) or vehicle control for the respective time points (6, 12, 24, 48 h). EPCs were characterized as adherent cells double positive for DiLDL-uptake and lectin binding by direct fluorescent staining under a laser scanning confocal microscope. EPCs proliferation, migration and in vitro vasculogenesis activity were assayed with MT assay, modified Boyden chamber assay and in vitro vasculogenesis kit, respectively. EPCs adhesion assay was performed by replating those on fibronectin-coated dishes, then adherent cells were counted., Result: Incubation of isolated human MNCs with puerarin dose increased the number of EPCs, maximum at 3 mmol x L(-1), 24 hours (approximately 1-fold increase, P < 0.01). In addition, puerarin also promoted EPC proliferative, migratory, adhesive and in vitro vasculogenesis capacity., Conclusion: Puerarin can augment the number of EPCs with enhanced functional activity.

Aim: To investigate whether puerarin can augment endothelial progenitor cells (EPCs) numbers, promote EPC proliferative, migratory, adhesive, and in vitro vasculogenesis capacity., Methods: EPCs were characterized as adherent cells by double staining of DiLDL-uptake and lectin binding under a laser scanning confocal microscope. Expression of KDR, VEGFR-2, and AC133 was detected by flow cytometry. EPCs proliferation, migration and in vitro vasculogenesis were determined with MTT assay, modified Boyden chamber assay, and in vitro vasculogenesis kit, respectively. EPCs adhesive assay was performed by replating those on fibronectin-coated dishes, then adherent cells were counted., Results: Incubation of isolated human MNCs with puerarin 0.1-3 mmol/L increased the number of EPCs, EPC proliferative, migratory, adhesive, and in vitro vasculogenesis capacity in a concentration- and time-dependent manner, which reached maximum at 3 mmol/L, 24 h (approximately 1-fold increase, P<0.01)., Conclusion: Puerarin enhanced EPCs functional activity.

The aim of the present study was to investigate whether fluvastatin augments the number of endothelial progenitor cells (EPCs), and promotes EPCs proliferation, migration and adhesion. Total mononuclear cells (MNCs) were isolated from peripheral blood by Ficoll density gradient centrifugation. The cells were then plated on fibronectin-coated culture dishes. After being cultured for 7 d, the attached cells were stimulated with fluvastatin (final concentrations: 0.01, 0.1, 1, 10 micromol/L), simvastatin (1 micromol/L) or a vehicle for the respective time points (6, 12, 24 and 48 h). EPCs were characterized as adherent cells double positive for DiLDL-uptake and lectin binding by direct fluorescent staining under a laser scanning confocal microscope. EPCs were further documented by demonstrating the expression of KDR, VEGFR-2 and AC133 with flow cytometry. EPCs proliferation, migration and in vitro vasculogenesis activity were assayed by MTT assay, modified Boyden chamber assay and in vitro vasculogenesis kit, respectively. EPCs adhesion assay was performed by replating it on fibronectin-coated dishes, and the adherent cells were then counted. In addition, we also studied EPCs culture assay of peripheral blood from fluvastatin-treated animals in vivo. Incubation of isolated human MNCs with fluvastatin dose- and time-dependently increased the number of EPCs, while reached the maximum 24 h after the administration at 1 micromol/L, (2.5-fold increase, P<0.05). Moreover, treatment of rats with fluvastatins elevated the number of EPCs (3-fold increase, P<0.05), thus extending the in vitro data. In addition, fluvastatin also promoted EPC proliferation, migration, adhesion and in vitro vasculogenesis in a concentration-dependent manner. The effects of fluvastatin on EPCs were compared with those of simvastatin at the same concentration (1 micromol/L), with a result of no statistical difference. The results of the present study define a novel mechanism of the action of statins: the augmentation of EPCs with enhanced functional activity.

Objective: To investigate whether hypercholesterolemia has influences on the number and activity of endothelial progenitor cells (EPCs)., Methods: Mononuclear cells were isolated from patients with hypercholesterolemia (n = 20) and age-matched control subjects (n = 20). EPCs were characterized as adherent cells double positive for DiLDL-uptake and lectin binding by direct fluorescent staining under a laser scanning confocal microscope. EPCs proliferation and migration were assayed by MTT assay and modified Boyden chamber assay, respectively. EPCs adhesion assay was performed by replating cells on fibronectin-coated dishes, then counting the adherent cells., Results: The number of EPCs was significantly reduced in patients with hypercholesterolemia as compared with that in control subjects [(41.8 +/- 8.7 vs 64.5 +/- 16.6) EPCs/x 200 fields; P < 0.05] and it was inversely correlated with total cholesterol levels (r = -0.659, P < 0.001) and LDL cholesterol levels (r = -0.611, P < 0.001). In addition, EPCs proliferative, migratory and adhesive capacity were also impaired., Conclusion: It is suggested that a novel pathophysiological mechanism of hypercholesterolemia may be defined i.e. reduction of EPCs with decreased functional activity.