AIM: This study was designed to investigate the secretion of VEGF and its receptor (flt-1 or flk-1/KDR) protein by cultured bovine thoracic aortic endothelial cells treated with various insulin concentrations. METHODS: Endothelial cells was isolated from bovine thoracic aorta, and cultured in serum-free medium, then incubated with different insulin concentrations (30 mU/L, 300 mU/L, 3 000 mU/L). The level of VEGF and its receptor (flt-1 or flk-1/KDR) protein were detected by immunohistochemical staining. RESULTS: As compared with no insulin group, the expression of VEGF protein in low insulin concentration (30 mU/L and 300 mU/L) groups were significantly increased (P0.05) was observed. CONCLUSION: Low concentration insulin up-regulates the VEGF protein expression, while high concentration insulin down-regulates the VEGF protein expression in bovine thoracic aortic endothelial cells, but insulin had no directly effect on the VEGF receptor (flt-1 or flk-1/KDR) protein expression in bovine thoracic aortic endothelial cells. [

0.05).However,other groups based on different extent and degree of pathology,clinical risk had significant difference in hs-CRP(P

0 05) between the insulin incubation groups both with and without L NAME incubations Conclusion Insulin has no direct effect on the expression of VEGF receptor (flt 1? flk 1/KDR) protein in bovine thoracic aortic endothelial cells The NOS 3 activation of endothelium is not the main cause that could affect the expression of VEGF receptor (flt 1?flk 1/KDR) protein of endothelium

AIM: To evaluate the method of inducing mouse embryonic stem (ES) cells in vitro to differentiate into cardiomyocytes without using any chemical reagents.METHODS: BRL conditioned medium was used to promote the growth of ES cells and maintain them in an undifferentiated state before the experiment of differentiation. Then a three-step method including ES cell culture in hanging drops and in suspending was used to induce the differentiation of ES cells. RESULTS: Rhythmically contracting cells were observed among differentiated cells, which were proved to be cardiomyocytes with electron microscope and immunocytochemistry. CONCLUSION: A simple and economical method was established to induce mouse ES cells cultured in vitro to differentiate into cardiomyocytes without using any chemical reagents. [

To investigate the protective effect of L-carnitine on myocardial ischemia-reperfusion injury in rat heart,all harvested isolated hearts were perfused on Langendorff apparatus with oxygenized K-H solution for 20 min. The hearts were then exposed to ischemia for 30 min. Following the ischemia the hearts were re-perfused with K-H solution for 120 min to serve as the control group A. Either 5 or 10 mmol/L of L-carnitine was added into the K-H solution for 20 min at the beginning of reperfusion to generate group B and group C, respectively. The derivatives of the intraventricular pressure curve (DP/DT), left ventricular developed pressure (LVDP), and coronary flux were monitored during the entire experiment. The levels of ATP, hepatin, malondialdehyde (MDA), and superoxide dismutase (SOD) in tissue, and lactic dehydrogenase (LDH), creatine phosphate kinase (CPK), malondialdehyde (MDA), and superoxide dismutase (SOD) concentration in the coronary efflux were all measured. Compared with the control group, the treatment with L-carnitine resulted in better results, i. e., higher DP/DTmax and LVDP. At the same time, ventricular fibrillation was reduced, and the levels of ATP, hepatin and SOD were all elevated. However, the concentrations of MDA, CPK and LDH were all reduced. In conclusion, L-carnitine has a protective effect on ischemia-reperfusion injury, which is partly due to its prevention of energy loss and its antioxidant activity.

Aim To determine the effects of sodium tashinoneⅡA sulfonate(TSN) on monophasic action potential(MAP) and tachycardia-induced electrical remodeling of rabbit atria in vivo.Methods Twenty-four rabbits were equally divided into two groups randomly: control group and TSN group.Electrical catheters were localized in the right atrium through right internal jugular vein.Right atrial MAP was recorded by multiple channel recording. ERP of right atrial(AERP) was assessed by programmed electrical stimulation before pacing and from 0～8 hours after the onset of the pacing.Results The AERP_(200 ms) of control group was shortened from (105.9?3.8) ms to(114.7?7.2) ms and the rate-dependent of control group's atrium was lost through the pacing process compared with TSN group before pacing(P

Aim To investigate the effect of fluvastatin(FV)on the expression of IL-1? mRNA of left ventricular(LV) myocardium in rats with heart failure after acute myocardial infarction(AMI).Methods 6 h after ligating left coronary artery,surviving AMI female SD rats were randomly assigned to: ①AMI control;②AMI+FV;③sham-operated group,which was randomly selected as non-infarction control.After 8 weeks of therapy,we assessed cardiac function,hemodynamics,ventricular remodeling parameters and IL-1? mRNA expression in the infarcted and non-infarcted area(IA,NIA).Results Compared with the sham-operated group,LV end-diastolic dimension(LVEDD),LV end-diastolic volume(LVEDV),E-wave,E-wave deceleration,E/A ratio,LV end diastolic pressure(LVEDP),relative weight(LVRW),right ventricular relative weight(RVRW),collagen volume fraction(CVF) and IL-1? mRNA in NIA were all significantly increased in the AMI group(all P

Objective By studying the expressions of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in rats′ cardiac muscle after acute myocardial infarction, we try to find out the relation between the expression of these two factors and the formation of new blood vessels under ischemia. Methods Wistar rats were divided into control group and infarction group (3, 7, 14, 28, 42, 56 d). The expression of VEGF and bFGF in cardiac muscle and endothelial cells is detected by means of immunohisto-chemial staining while the density of newly formed ressels is detected by marking the endothelial cells with antigens associated with factor Ⅷ. Results After ligating the left anterior descending coronary artery of the rats, the expression of VEGF and bFGF increased along with the prolongation of myocardial ischemia and reached the peak on the 7th day. The expression of the 2 factors began to decrease on the 28th day and the most significant decrease happened on the 42th and 56th day. The density of the newly formed capillaries is directly propontimal to the levels of the 2 factors. Less expression of VEGF and bFGF was observed in the control group. Conclusion The up-regulation of VEGF and bFGF expression might play important roles in neovascularization. Dicrectly intramyocardial injection of bFGF and VEGF gene at the time when the expression of bFGF and VEGF began to decrease maybe optimal.

Objective To study the therapeutic effect of mobilization of autologous bone marrow stem cells by G-CSF on myocardial infarction in experimental rats. Methods Rat model were established by coronary ligation. Rat bone marrow stem cells were mobilized by G-CSF. The volume of CD34~+ cells in peripheral blood was examined 1 week after myocardial infarction by flow cytometry. The infiltration of CD34~+ cells in the infarct zones were detected by immunohistochemical methods. At 4 weeks after infarction, the size of the infarction area, capillary density and cardiac function were evaluated by means of HE and immunohistochemisty staining as well as hemodynamic measurements. Results After 1 week, the level of CD34~+ cells in the G-CSF group increased significantly compared with the control group and infiltration of CD34~+ monocytes were found in the junctional zones in the G-CSF group. After 4 weeks, the size of the infarction area was minimized in the treatment group. More angiogenesis and better cardiac function were found in the G-CSF group compared with the control group. Conclusion The therapy of mobilization of autologous bone marrow stem cells by G-CSF is effective in treatment of myocardial infarction in rat models.