Objective To observe the effect of grape seed Procyanidins on platelet aggregation and experimental thrombosis in rats.Methods 50 Experimental thrombosis male SD rats of clean grade,weighing 250～300 g,were randomly divided into five groups,normal saline(control)group,aspirin(ASP)group(60 mg/kg),and procyanidins 1 00 mg/kg,200 mg/kg,400 mg/kg group,10 in each.50 experimental thrombosis male Kunming mice of clean grade,weighing 18～20 g,were also randomly divided into five groups,normal saline(control)group,aspirin group(84 mg/kg)and Procyanidins 140 mg/kg,280 mg/kg,560 mg/kg group,10 in each.Intragastric administration was performed in these experimental animals.The effects of Procyanidins were observed on rat platelet aggregation induced by ADP,COL and AA.Experimental rat's thrombosis was induced by method of"arterio-venous"shunt and the death rate within 15 min was determined with collagen plus adrenaline induced thrombus model in mice,aspirin as a positive control.Results Procyanidins in the middle and high-dose group can inhibit ADP,COL,AA-induced platelet aggregation and experimental thrombosis obviously.Conclusion Procyanidins can inhibit experimental thrombosis and have anti-platelet aggregation effect.

The fetal spleen cells were transplanted following the injection of S180 carcinosarcoma into the muscle,abdominal cavity,peripheral veins and portal vein in mice.The size inhibitory rate of the transplanted tumor and natural killer activity were evaluated 30 and 60 days after the injection.It was found that the growth of transplanted tumor was dramatically inhibited and natural killer activity was increased 30 days after the transplantation.But 60 days after the transplantation only portal venous transplanted tumor showed a satisfactory function of inhibiting tumor growth and natural killer activity maintained at a high level.These results indicated that portal vein was the best approach for the spleen cell transplantation

Aim To investigate the alteration of Wnt/β-catenin signaling pathway in early diabetic rat myo-cardium and clarify its role in development of diabetic cardiomyopathy. Methods The diabetes mellitus ( DM) model was prepared by intraperitoneal injection of streptozotocin ( STZ, 60 μg · g-1 ) . The alteration of Wnt/β-catenin signaling pathway was determined by Western blot and immunohistochemistry. HE staining was used to analyze the change of myocardial pathologi-cal structure. Results Cardiac histological analyses revealed that DM induced cardiomyocyte degeneration and necrosis. Myocardial Wnt2, β-catenin and c-Myc were enhanced in 2 wk DM compared with control group while DKK1 showed no significant alteration. Conclusion Wnt/β-catenin signaling pathway is acti-vated in early diabetic myocardial injury. Further re-searches on its role in DM myocardium may find a new therapeutic target for diabetic cardiomyopathy.

AIM: The purpose of this study was to evaluate the mechanism of high altitude pulmonary edema (HAPE) and high altitude acute response (HAAR). METHODS: Pulmonary function and partial oxygen pressure were measured in 10 patients with HAAR and 6 patients with HAPE before and after bronchoalveolar lavage (BAL),10 high altitude healthy volunteers were served as control subjects. RESULTS: The partial oxygen pressure of HAAR and HAPE significantly decreased before BAL compared with control; DLCO%, DLCO/VA%, PaO_2 of HAPE increased significantly [from 76.01%?6.29%, 150.30%?15.20%, (31.73?3.01) mmHg before BAL to 103.31%?9.23%, 176.04%?16.10%, (45.31?3.56) mmHg after BAL]. The above parameters were also changed in HAAR and controls, but had no statistical significance. CONCLUSION: High concentration of proteins and cells in BAL fluid for HAPE, gas exchange impairment and PaO_2 increase after BAL suggest accumulation of protein-rich fluid and cells in the alveolar space plays a crucial role in the development of HAPE.

BACKGROUND: Hippocampal neuron presents remarkably injury in cerebral after seizure of epilepsy. Necrosis and apoptosis are two kinds of neural cell injury after epilepsy and play an important role in neural injury of epilepsy. Being endogenous neural protective transmitter, adenosine may inhibit the release of excitatory amino acid, production of oxygenic free radical and action of nitric oxide. Simultaneously, it can improve cerebral blood flow and anti-convulsion. But it has been unknown concerning to the relationship between adenosine and cell apoptosis after epilepsy yet.OBJECTIVE: To observe the effects of 2-CAdo adenosine-receptor excitant on genetic expression of bcl-2, Bax of hippocampal cells in epileptic rats and further probe into the mechanism of adenosine on anti-convulsion and brain protection.DESIGN: Completely randomized controlled experimental research in which the experimental animals were taken as the objects.SETTING: Pediatrics department and general surgical department of one oil field general hospital, and pediatric internal department of a hospital affiliated to one university.MATERIALS: The experiment was performed in Experimental Zoology Departnent and Pathological Teaching & Research Department of Harbin Medical University from October 2002 to March 2003. Totally 104 Wistar rats of either sex were employed, weighing varied from 200 g to 250 g. The animals were randomly divided, named as normal group 8 rats, epileptic group 32 rats, epileptic & 2-CAdo group 32 rats, and epileptic & physiological saline group 32 rats.INTERVENTIONS: The animal epileptic model was set up by intra-abdominal injection of coriamyrtin 15 mg/kg(provided by Pathology Department of Harbin Medical University. Convulsion presented in all of rats, 5 minutes later after injection, lasting for 1 or 2 minutes. In epileptic & 2-CAdo group, 2-CAdo(provided by ICN company), 0.6 mg/kg, was injected from the vein on the tail 1 hour before coriamyrtin injection and 1 hour after convulsion respectively. In epileptic & physiological saline group, the physiological saline of equal dosage was injected from the vein on the tail 1 hour before coriamyrtin injection and 1 hour after convulsion respectively.MAIN OUTCOME MEASURES: Positive cell counts of bcl-2 and Bax genetic expression in hippocampal CA1 area.RESULTS: Twenty-four hours after epilepsy seizure, neural cell bcl-2 expression was increased in hippocampal CA1 area, was remarkably decreased in 48 hours, and the expression was only little amount in 72 hours, but it was increased again in 7 days. Bax expression began increased in 24 hours after epilepsy seizure, was significantly increased in 48 hours, reached the peak in 72 hours, the expression was the minimum in 7 days. In epileptic & 2-CAdo group, bcl-2 expressions at corresponding times were remarkably increased compared with epileptic group and epileptic & physiological saline group( P＜ 0.05), Bax expressions were remarkably decreased compared with epileptic group and epileptic & physiological saline group( P ＜ 0.05), indicating statistical significance.CONCLUSION: 2-CAdo can reduce apoptosis of hippoeampal neural cells after epilepsy seizure and provide a certain protection for neural cells.

Aim To investigate the alteration of Wnt/β-catenin signaling and sirtuins 1 in type 2 diabetic rats’ aorta and clarify its role in the development of di-abetes aortic disease. Methods The type 2 diabetes rat model was established by injection of streptozocin after five-week of high fat diet. The rats were randomly divided into control group, DM model group of 2 weeks, 4 weeks, 8 weeks and 12 weeks. Fasting blood glucose ( FBG ) , total cholesterol ( TC ) , triglyceride ( TG) , high density lipoprotein-cholesterol( HDL-C) , low density lipoprotein- cholesterol ( LDL-C ) and fast-ing insulin( FINS) levels were tested. HE staining was used to observe the pathological changes of aortal struc-tures. The alteration of Wnt2, β-catenin, TCF4, SIRT1 and sFRP2 in aortawas determined by Western blot and RT-PCR. Results Compared with control group, TC, TG, LDL-C levels of type 2 diabetic rats were significantly increased, HDL-C levels were signif-icantly reduced( P<0. 01 ) . Aortic histological analy-sis revealed that DM induced aortic endothelial cell vacuolar degeneration and necrosis. The expression of Wnt2 and β-catenin level increased significantly in the first 4 weeks of diabetic groups compared to control group, and that in model group of 8 weeks and 12 weeks kept in the high level and showed no significant alteration(P>0. 05). But the expression of TCF4 and SIRT1 was enhanced continuously in DM compared with control group while sFRP2 decreased in the duration of DM development. Conclusions Wnt/β-catenin signa-ling pathway was activated in diabetic aortal injury by regulation of SIRT1 via sFRP2 . Further researches on its mechanism of actionin DM aorta injury may find a new therapeutic target for the disease.

Objective To investigate ACEI ( benazepril ) and tranilast exert renoprotective properties in diabetic nephropathy( DN) through the inhibition of thioredoxin( Trx) . Methods Forty male SD rats were randomly divided into normal control group,model control group,tranilast group and benazepril group (n=10 each).Normal control group was fed with normal diet. Other groups were fed with high-glucose high-fat diet to make DN models. Rats in model control, tranilast, and benazepril groups were fed with normal diet,400 mg??kg-1??d-1 tranilast plus normal diet,and 10 mg??kg-1??d-1 benazepril plus normal diet,respectively,via oral gavage for 12 weeks.The 24-hour proteinuria,blood glucose(BG),blood urea nitrogen (BUN),serum creatinine ( Scr) and renal pathology changes were detected. Expression of Trx was measured by Western-blot. Results The 24 h urine protein, BG, BUN, Scr, kidney/body weight, and glomerular sclerosis index were significantly decreased in tranilast group and benazepril group,as compaired with model control group ( P<0.05) ,but there was no statistical difference between the two drug groups (P>0.05).Both tranilast and benazepril can reduce renal pathological changes,and can increase the expression of Trx of DN rats, but benazepril had a more significant effect on increasing Trx expression. Conclusion Both tranilast and benazepril have renoprotective function in DN, and benazepril is more effective than tranilast in delaying the progression of diabetic nephropathy by increasing Trx expression and decreasomg oxidative stress.

Objective To observe the changes of peripheral blood interleukin-2(IL-2) ,interleukin-4(IL-4) ,interleukin-10(IL-10) ,tumor necrosis factor-alpha(TNF-α) and interferon gamma (IFN-γ) in chronic hepatitis B(CHB) patients with positive e-anti-gen(HBeAg) treated by Bushenqingtou Decoction .Methods 60 cases of CHB with positive HBeAg were randomly divided into the treatment group and the control group ,30 cases in each group .The CHB treatment group received Bushenqingtou Decoction with the treatment course of 48 week ,while the CHB control group did not received the medication therapy .In the beginning and at 48 weeks of treatment ,the blood in the two CHB groups were collected for detecting HBV DNA ,IL-2 ,IL-4 ,IL-10 ,TNF-αand IFN-γ. Results Compared with before treatments ,the levels of IL-2 ,TNF-αand IFN-γafter treatments in the CHB treatment group were obviously increased ,while the levels of HBV DNA ,IL-4 and IL-10 were remarkably decreased (P<0 .01);however ,there were no statistical differences of the various indexes after the treatments in the CHB control group (P>0 .05) .Conclusion Bushenqingtou Decoction could inhibit the replication of HBV DNA in the CHB patients with positive HBeAg and improve the body immune func-tion .

Aim To explore the protective effects of LPPC ( procyanidins extracted from the litchi pericarp) on cardiomyocyte apoptosis in septic rats and its mech-anisms. Methods The rats were randomly divided in-to 5 groups, and were given orally the drug for two weeks continuously. The control group ( control) and sepsis model group ( LPS ) were given distilled water once a day. LPPC low, medium and high dose groups were given LPPC 50 , 100 , 200 mg · kg-1 · d-1 re-spectively which were prepared freshly every day. After the treatment, sepsis animal models were established. Except for the control group, other groups were injec-ted LPS (lipopolysacchride, 10mg·kg-1) intraperito-neally to induce acute sepsis model. 4hrs later, rat se-rum was collected, isoenzyme ( CK-MB ) , lactate de-hydrogenase ( LDH ) and activity of aspertate amin-otransferase ( AST/GOT) were detected. Then rat car-diac tissue was obtained and cardiac tissue malondial-dehyde ( MDA ) , total antioxidant capacity ( T-AOC ) and reduced glutathione ( GSH ) content were deter-mined. TUNEL staining was performed to analyze the apoptosis of myocardial cells. Cleaved caspase-3 and TNF alpha protein expressions were analyzed by West-ern blot. Results Compared with the control group ( control) , serum of sepsis model group rats CK-MB, LDH, AST/GOT and cardiac tissue MDA content were significantly increased (P<0. 01). At the same time, the activity of cardiac tissue T-AOC and GSH de-creased obviously ( P<0. 01 ) . The apoptotic myocar-dial cells increased significantly ( P<0. 01 ) , and the expression level of cleaved caspase-3 and TNF alpha decreased obviously ( P <0. 01 ) . LPPC pretreatment significantly decreased the serum CK-MB, LDH, AST/GOT and tissue MDA content, increased tissue T AOC and GSH activity, attenuated apoptosis of rat myocardi-al cells significantly, and decreased expression level of cleaved caspase-3 and TNF alpha. Conclusion LPPC pretreatment can significantly attenuate rat myocardial cell apoptosis induced by sepsis, and the underlying mechanisms may be related to its anti-oxidative effects.

Aim To study the mechanisms of the pro-tective effect of procyanidin B2 ( PCB2 ) on the myocar-dial cell apoptosis induced by lipopolysaccharide ( LPS) . Methods Using the primary culture rat myo-cardial cells, myocardial cell injury model was induced by LPS. PCB2 low, medium and high dose groups, were cultured with 6. 25 , 12. 5 , 25. 0 μmol · L-1 PCB2 respectively in DMEM medium for 24 h continu-ously. Myocardial cell survival rate was determined by MTT colorimetric method. Cardiacmyocyte NOX activi-ty was determined by lucigen chemiluminescence meth-od . Western blot analysis was used to detect myocardi-al NADPH oxidase p47phox expression. TUNEL method was used to detect apoptosis and flow cytometry was used to determine the content of myocardial cells ROS. Results Compared with control group, the cell dam-age induced by LPS group myocardial cell survival rate significantly decreased ( P <0. 01 ) , and myocardial cell NOX activity, p47phox expression, apoptotic cell number and ROS content were significantly increased (P<0. 01). PCB2 low, medium and high dose groups cell survival rates were significantly elevated, myocar-dial cell NOX activity and p47phox expression, apoptotic cell number and the ROS content decreased significant-ly in a dose-dependent manner ( P <0. 01 ) . Conclu-sion PCB2 protects myocardial cell apoptosis induced by LPS via inhibiting the expression of NADPH oxidase activation, p47phox expression and reactive oxygen spe-cies generation.