Blood viscosity, plasma viscosity, haematocrit and electrophoresis time of red blood cell and platelet were raeasured before and 24h after operation, in which 8 rabbits were AMI, and 8 with the coronary arteria not ligated as control. The AMI group had significantly higher adjusted viscosity and electrophoresis time of red cell and platelet than the control group (P

The effects of DMSO and nifedipine on experimental myocardial infarction induced by isoproterenol(ISP)were investigated.The results showed a significant reduction in myocardial FFA and MDA contents in DMSO and nifedipine-treated groups, as compared with the ischemic group, and a beneficial effect on activity of SOD,GSH-px and Ca~(2+)-Mg~(2+)-ATPase. The effects of OH. and Ca~(2+) in myocardialg infarction were further analysed in this study.

The changes of lipid peroxidation in the ischemic (renal artery occlusion for 75 min) and ischemie/reperfusion (renal artery occlusion 60 min plus 15 min reflow) kidney was studied in 19 male SD rats. The results showed that malondialdehydc of renal cortex and medulla was increased, but in both groups SOD and GSH-Px were not changed significantly. Activity of xanthine oxidase activity in the ischemic/reperfusion kidney were increased as compared with normal. These results suggest that lipid pcroxidation was involved in the ischemic and ischemic/reperfusion renal injury, and xanthine-xanthine oxidase might be one of the major sources of oxygen free radical when oxygen supply to ischemic kidney was restored.

AIM: To investigate the effect and mechanism of Astragalus polysaccharide (APS) on the amelioration of hepatic insulin resistance in high fat-fed mouse model.METHODS: C57BL/6J mice (n=26) were divided into three groups randomly: C group (an animal model for control, n=10); IR group ( an animal model of insulin resistance, n=8) and IA group (an animal model in high-fat diet with APS treatment for12 weeks, 700mg?kg-1?d-1, ig). High-fat diet was used to induce the formation of insulin resistant. The parameters and insulin sensitivity of the animals were observed. The pathological features of the liver were presented through microscope and TEM. The expression changes of hepatic GSK3? were measured by Western blotting.RESULTS: In this study, the fat-fed mouse model of insulin resistance was established successfully. The mice in IA group responded to the 12-week APS therapy with a significant decrease in the level of blood glucose, plasma insulin, body weight, hepatic TG/FFA and improved glucose tolerance compared with those in IR group. In addition, the expression and the activity of GSK3? were lower in IA group (vs IR group,P

AIM: To investigate the effect of vasodilator-stimulated phosphoprotein (VASP) phosphorylation on the cell migration induced by platelet-derived growth factor BB (PDGF-BB), and to identify which phosphorylation site was more important among the three phosphorylation sites, namely Ser157,Ser239 and Thr278. METHODS: Two phosphorylation mutants of VASP, pcDNA3.1(+)/VASP-S157A and pcDNA3.1(+)/VASP-S239A, were constructed and respectively transfected into the cultured ECV304 cells by means of liposome. The stable expression cells were screened by using antibiotic G418. Protein expression of VASP was measured by Western blotting. The ECV304 cell migration was evaluated using Transwell chamber. RESULTS: Compared to control group, the cell migration was significantly inhibited in ECV304 transfected with VASP-S157A and VASP-S239A (P<0.05), although slight differences existed between VASP-S157A and VASP-S239A transfected cells (P>0.05). CONCLUSION: VASP mutation on the phosphorylation sites of Ser157 and Ser239 inhibits cell migration, and the phosphorylation sites of Ser157 and Ser239 both greatly affect the function of VASP.

Objective To investigate the ameliorative effect and a mechanism of APS on the hepatic steatosis in diabetic KKAy mice.Methods KKAy and C57BL/6J mice were respectively seperated into KK and K+A(n=8)as well as C and C+A(n=10)groups.Blood and hepatic biochemical parameters were observed.Insulin sensitivity was analyzed by OGTT & HOMA-IR.Hepatic pathological changes were presented through microscope and TEM.The expressions of hepatic GSK3? and insulin-induced Ser9GSK3? were performed by Western blot.Results With 8-week APS therapy in K+A group,the levels of blood glucose and hepatic TG and FFA were decreased,insulin sensitivity was improved,the hepatic steatosis was significantly alleviated(P

Objective To explore the protection effects of the reduced form of nicotinamide-adenine denucleotid(NADH) on cardiac fibroblasts apoptosis induced by hydrazine in vitro.Methods Cardiac fibroblasts isolated from neonate rats were divided into four groups.In NADH pretreatment before hydrazine treatment group,the cardiac fibroblasts were cultured first in the medium containing 400?g/ml NADH for 2 hours,and then cultured in the medium containing 400?g/ml NADH plus 2mmol/L hydrazine for 72 hours;in hydrazine treatment group,the cardiac fibroblasts were cultured first in normal medium containing 400?g/ml NADH for 2 hours and then cultured in the medium containing 2mmol/L hydrazine for 72 hours;in control group,the cardiac fibroblasts were cultured only in normal medium for 72 hours;and in NADH pretreatment control group,the cardiac fibroblasts were cultured in medium containing 400?g/ml NADH for 72 hours.After the treatments mentioned above,the changes in nuclear of apoptotic cardiac fibroblasts as stained by Hoechst33258 were observed under fluorescence microscope,the apoptotic and necrosis rates of cardiac fibroblasts stained by AnnexinⅤ/PI were assayed by flow cytometry,the mitochondria membrane potential of cells stained by rhodamine123 was also assayed by flow cytometry.Results Hydrazine could induce apoptosis of the cardiac fibroblasts.After NADH pretreatment,the number of apoptotic cardiac fibroblasts with pyknosis of nuclear was lowered,the rates of apoptosis and necrosis decreased,and the mitochondria membrane potential of cells was elevated.Conclusion NADH pretreatment could reduce the apoptosis induced by hydrazine by improving the function of mitochondria.

BACKGROUND: The structural and functional impairment of endothelium cells were mainly presented by lowered endothelium activity, reduced nitrogen monoxide production, as well as increased endothelium vasoconstrictor peptide (EVCP).OBJECTIVE: To study the protective role of astragalus polysaccharide on atherosclerosis induced by eudothelium cell injury, which was compared with that of Captopril.DESIGN: Randomly controlled observation.SETTING: Department of Physiology, Hubei College of Traditional Chinese Medicine; Department of Pathophysiology, Medical College of Wuhan University;Department of Surgery,Hetang Hospital of Guangdong Province;Department of Endocrinopathic Sciences,Renmin Hospital,Wuhan University.MATERIALS: The study was carried out at the Organic Function Laboratory of Hubei College of Traditional Chinese Medicine and the Pathophysiological Department of Wuhan Medical University from July 2001 to December 2002. Forty healthy male rabbits provided by the experimental animal center of Wuhan medical university, weighed of 2.4-3.0 kg, were randomly divided into blank group,model control group,astragalus polysaccharide group and captopril group with 10 rabbits in each group.Astragalus polysaccharide was extracted from Shanxi produced astragalus root and made into injection powder that should be freshly composed with physical saline before usage.METHODS: Rabbits in blank group were raised with granular feed, while rabbits in other three groups were given hyperlipid feed (80％ basal feed mixed with 15％ yolk powder, 0.5％ cholesterin and 5％ lard), in addition with venous injection of bovine serum by 1 mL/kg once, atherosclerosis induced endothelium injury model was established on rabbit by hyperlipid feed combined with immune injury. Rabbits in astragalus polysaccharide group received intraperitoneal injection of polysaccharide of 500 mg/kg once a day; which replaced by 5 mg/kg captopril in captopril group that equals to 5 times clinical dosage; While rabbits in blank group and model control group were given the same volume physical saline of 4 mL/kg for totally 50 days. Blood were collected from SVC 24 after the last medication and then rabbits were put to death, the morphological changes of abdominal aorta were observed under optical microscope, meanwhile the changes of serum total cholesterol, triglycerides, nitrogen monoxide, EVCP, superoxide dismutase, malonaldehyde and total antioxidation activity were examined.MAIN OUTCOME MEASURES: ① Morphological changesof abdominal aorta. ② Changes of serum parameters.RESULTS: All 40 rabbits complete the experiment without loss. ① In contrast with model control group group, the total serum total cholesterol and triglycerides in astragalus polysaccharide group and captopril group obviously decreased [(9.33±1.13), (6.60±0.61), (7.09±0.74) mmol/L, P ＜ 0.05;(3.05±0.44), (1.26±0.16), (2.17±0.46) mmol/L, P ＜ 0.01, P＜ 0.05],malonaldehyde and EVCP markedly decreased [(9.98 ± 1.11 ), (7.10 ±0.68),(9.46±1.27) μmol/L, P ＜ 0.01; (741.90±34.98), (632.62±26.95),(600.74±32.59) ng/L, P ＜ 0.01]. ② Comparing to model control group group,the serum nitrogen monoxide and superoxide dismutase were obviously increased in astragalus polysaccharide group and captopril group ·[(11.04±1.68),(19.96±6.05), (18.35±3.52) μmol/L, P ＜ 0.01, P ＜ 0.05; (159.32±5.26),(207.54±16.98), (197.59±28.41) NU/mL, P ＜ 0.0l, P ＜ 0.05], the total antioxidation activity also increased [(23.8±3.5), (34.7±5.6), (30.7±6.8)％,P ＜ 0.01, P ＜ 0.05]. ③ Either the decrement of serum triglycerides, total cholesterol and malonaldehyde or the increment of nitrogen monoxide, superoxide dismutase and total antioxidation activity in astragalus polysaccharide group was greater than captopril group (P ＜ 0.01). ④ Morphological changes of abdominal aorta: The aorta intima was smooth and endothelium cells were continuous with small intervals between cells in blank control group,endothelium cells presented normal configuration without edema;while intima in model control group became thick and upheaved, part of endothelinm cells detached with widened intervals. The media became thickened with leiomyocyte displaying hyperplasic and infiltering into endothelium, foaming cells could also be observed; the aorta intima was smooth and endothelium was closely connected in astragalus polysaccharide group, the hyperplasia of leiomyocyte was not active and foaming cells seldom observed; while in captopril group, the aorta intima was smooth without obvious detachment of endothelium cells and infiltration of leiomyocyte, leiomyocytes were normal and ranked orderly.CONCLUSION:Astragalus polysaccharide could markedly eliminate serum triglycerides, total cholesterol, malonaldehyde and EVCP, thereby alleviate vascular impairment induced by EVCP, meanwhile markedly increased serum nitrogen monoxide, superoxide dismutase and total antioxidation activity, the intima surface of abdominal aorta could be smooth due to the administration of AP, endothelium configuration would be basically complete, implying that it has better antioxidation property and protective role for endothelium cells.

AIM: To study the role of calcineurin (CaN)-dependent signaling pathway in proliferation of vascular smooth muscle cells (VSMCs) by observing the effect of cyclosporin A (CsA) on proliferation of neuropeptide Y (NPY)-induced rat VSMCs. METHODS: Upon the model of cultured rat VSMCs, the study consisted of three groups: NPYgroup,CsA+NPY group and control group. CaN activity was determinated by enzyme reaction phosphorus measurement. The methods of biochemistry (MTT) and quantitative immunocytochemistry were applied to investigate the proliferation of VSMC and the expression of proliferation cell nuclear antigen (PCNA) in cultured rat VSMCs. (RESULTS:) (Compared) with the control group, the VSMC's CaN activity, proliferation activity and expression of PCNA (by photo densitometry A_(PCNA)) were obviously increased in NPY group (P

AIM:To investigate the injurious effects of oxidized low-density(OLDL) on human endothelial cells(ECs) and protective effects of Angelica Sinensis in vitro. METHODS: The effect of OLDL on nitric oxide (NO) release from EC and intercellular adhesion molecule-1 (ICAM-1) expression on EC surface were studied, and the protective effects of Angelica Sinensis on normal and abnormal EC were investigated using cultured EC with or without OLDL and immunocytochemical staining technique. RESULTS: OLDL led to a decrease of NO release and an increase of ICAM-1 expression, which can be reversed by Angelica Sinensis and atropine can block this role of Angelica Sinensis. CONCLUSION: Angelica Sinensis has antagonistic effect on OLDL-induced decreasing of NO released from ECs and increasing of ICAM-1 expression on ECs surface . These effects of Angelica Sinensis may be exerted by the excitation of muscarinic receptor.