Aim To investigate the effects of pumpkin polysaccharide(PP) on Fas、Fas-L、Bcl-2 and Bax expression in the pancreas of diabetic rats.Methods Rats were injected intraperitoneally(ip) with streptozocin(STZ) 60 mg?kg-1 to induce diabetic model.The diabetic rats were given PP 150 mg?kg-1,300 mg?kg-1,600 mg?kg-1.The blood sample were taken after three weeks.Blood glucose was measured by glucose oxidase method;The expression of the Fas and Fas-L have been determined by using immunohistochemistry(S-P method);The expression of Bax mRNA and Bcl-2 mRNA were checked up by Reverse transcription PCR(RT-PCR).Results PP could decrease the level of blood glucose in streptozotocin-induced diabetic rats;After three weeks,The expressions of the Fas and FasL in ? cell of streptozotocin-induced diabetic rats were obviously lower;The expression of Bax mRNA was obviously down-regulated,the expression of Bcl-2 mRNA was obviously up-regulated,and the ratio of Bcl-2/Bax was advanced after the diabetic rats were given PP.Conclusions PP could decrease the level of blood glucose of the diabetic rats.The mechanism was related to decreasing the expressions of the Fas and FasL and regulating the expressions of Bcl-2 and Bax in the pancreas of diabetic rats.

Aim To investigate the relationship between oxidative stress and the aortic endothelial cells injury in type 2 diabetes rats,as well as the effect of valsartan. Methods The type 2 diabetic models were induced by low dose of streptozotocin (STZ) with high-energy diet.12 weeks after injecting STZ, rats were randomly divided into three groups: normal control, diabetes control and valsartan (24 mg?kg-1?d-1, 8 weeks, ig.) treated diabetes. At the 12th and 20thweek end, such indices as the endothelium-dependent vasodilation and the shape of aorta endothelium, the serum contents of SOD, GSH-Px , MDA and NO, and the level of NOS gene expression in aorta were measured. Results ① At the 12th weekend,in the diabetes group, the relaxation of aortic rings to low concentration of Ach declined, the aortic endothelial cells intumesced, contents of serum SOD, GSH-Px, MDA and NO significantly increased, the expression of iNOS mRNA in aorta obviously up-regulated while the expression of eNOS mRNA showed no change. ② At the 20th weekend,in the diabetes control group, the dilatory reactivity of aortic rings decreased to each concentration of Ach, the aortic endothelium appeared degenerative and necrotic, activities of SOD and GSH-Px decreased as well as the content of NO, the content of MDA increased continuously, and the iNOS mRNA expression up-regulated while eNOSmRNA expression down-regulated. Valsartan could regress the aggravation and improve contents of serum SOD, GSH-Px, MDA, NO and NOS mRNA of the aorta. Conclusion The oxidative stress and abnormality of NO participate the process of aortic endothelial cell injury. Valsartan plays a protective role partially through enhancing antioxidation effect and adjusting NO production.

Aim To investigate effects of moxonidine on hemodynamics in anesthetized rats. Methods The indexes of hemodynamics were examined by catheterization of arteries in anesthetized Wistar rats. Results DBP, +dp/dt_ max, -dp/dt_ max,t-dp/dt_ max ,V_ pm and V_ max were significantly declined in dose-dependent manner after administration, but HR and SBP didn't change significantly. Conclusion These results showed that antihypertensive effects of moxonidine were related to inhibition of systolic and diastolic functions of myocardium.Furthermore,the antihypertensive effects of moxonidine were associated with reduction of peripheral vascular resistance.

The phospholipase A2 ( PLA2 ) is one of the main constituents of the bee venom. Its hypotensive effect and mechanism are studied in this report.In the anaesthetized rats and cats, the PLA2 of the bee venom given intravenously caused a quick and profound fall in the arterial blood pressure.The results of this study indicate that its hypotensive effect is mainly concerned with releasing the endogenous histamine. If the antagonists of H1 and H2 receptor are administered together, its hypotensive action will be countered.

Aim To investigate the effect of irbesartan and spironolactone on expressions of connective tissue growth factor(CTGF),P-p38MAPK proteins during vascular remodeling in renovascular hypertensive rats(RHR).Methods Renovascular hypertension was induced by two kidney one clip(2K1C)operation.8 weeks later,RHRs were given irbesartan or(and)spironolactone for 8 weeks.After 8 weekstreatment,the morphometric measurements were performed in the mesenteric arterioles.Concertration of carboxyterminal propeptide of typeⅠprocollagen(PⅠCP)and N-terminal propeptide of type Ⅲ procollagen(PⅢNP)in blood serum was measured by enzyme linked immunosorbent assay method,and the media collagen area was assessed by collagne-specific Picro-sirius red staining with computerized video processing.Expressions of collagen type I,CTGF,P-p38MAPK proteins were detected using immunohistochemistry respectively.Results The arterial systolic pressure was attenuated significantly after the treatment of irbesartan,and this effect could not be enhanced by spironolactone.The media thickness over lumen ratio,media cross-sectional area over luminal area ratio of mesenteric arterioles,concertration of PⅠCP and PⅢNP,media collagen area,and expression of collagen typeⅠwere significantly increased in RHRs but ameliorated by irbesartan and spironolactone.Meanwhile,the expressions of CTGF,P-p38MAPK proteins were up-regulated in RHRs but blunted significantly after the treatment of irbesartan and spironolactone.The combined treatment had the synergic effects.Conclusions There is a synergistic effect of attenuating extracellular matrix(ECM)producing and amelioration of vascular remodeling(VR)by combined use of irbesartan and spironolactone.It maybe related to the expressions of CTGF and P-p38MAPK proteins down regulated by these two drugs.

Aim To investigate the myocardial hypertrophy,the expression of transforming growth factor ?1(TGF-?1),Smad3 and Smad7 proteins in spontaneous hypertensive rats(SHR)and the effects of benazepril and candesartan.Methods SHRs of 12 weeks old were given benazepril and candesartan for 12 weeks.The tail arterial pressure was measured every two weeks.At 12 th weekend,cardiac configuration,heart mass index,area of cadiocytes,concertrations of AngⅡin plasma and myocardium,expressions of TGF-?1、Smad3 and Smad7 proteins were measured respectively.Results The arterial pressure,wall thickness,heart mass index,area of cardiocytes and the expressions of TGF-?1,Smad3 proteins increased in SHRs but were attenuated after the treatment of benazepril or candesartan.After the combined treatment,the synergistic effect could be observed.The levels of cardiac tissue and plasma AngⅡwere reduced.The expressions of Smad 7 were up-regulated after the treatment of benazepril or candesartan,while they were stable after the combined use.Conclusion There is a synergistic effect of attenuating myocardial hypertrophy in SHRs by combined use of benazepril and candesartan.It may be related to the regulation of Ang Ⅱ,decreasing the expressions of TGF-?1 and Smad3.

AIM: To investigate the alteration of the vascular response to contracting material and the endothelium dependent vascular relaxation (EDVR) at different stages of type Ⅱ diabetes rats. METHODS: Type Ⅱ diabetes rat model was established by high-energy diet and lower dose of STZ. At 12th and 20th weekends after injecting STZ, the vascular reactivities to phenylephrine (PHE) and KCl and the EDVR induced by Ach were measured respectively in the isolated aorta rings. RESULTS: At 12th weekend after injecting STZ, the response to PHE increased, the reactivity to KCl kept unchanged, and the EDVR was damaged lightly. But at the 20 th weekend after injecting STZ, the response to PHE increased further and the reactivity to KCl markedly reinforced, and the EDVR was obviously damaged. CONCLUSION: The response of great vessels to contracting material increased, but the EDVR attenuated at different stages of type Ⅱ diabetes rats. These changes are further reinforced along with the developing of disease duration.

AIM: To study the expression of type Ⅰtransforming growth factor ?(T?R-Ⅰ)in renal cortex in streptozotocin-induced type Ⅱ diabetic mellitus and the regulation of valsartan. METHODS: The rat models of type Ⅱ diabetic rats were made. At the end of the 20th weeks,the kidneys were taken out to measure the expression of T?R-ⅠmRNA by RT-PCR. RESULTS: The expression of T?R-ⅠmRNA in diabetic rats without any therapy ( 0.72? 0.14) was higher than that in control ( 0.26? 0.12) (P

Aim To investigate the alteration of the nitric oxide (NO), the expression of nitric oxide synthase (NOS) mRNA at different stages of the cardiomyopathy in type 2 diabetes rats, and the protective effects of valsartan. Methods Type 2 diabetes model was established by high-energy diet, lower dose of STZ treated SD rat. The treatment period of valsartan was 8 weeks. At 12th and 20th weekend after injection of STZ, cardiac function, heart weight index, concentrations of NO in myocardium and plasma, expressions of iNOSmRNA and eNOSmRNA were measured respectively.Results From 12th week to 20th weekend, the left ventricular systolic and diastolic function was decreased and the heart weight index was increased in diabetes control group (DC group) compared with normal control group (NC group). The levels of the cardic tissue and plasma NO were higher at 12th weekend and lower at 20th weekend in DC group than that in NC group. The expression of iNOSmRNA in cardiac tissue was obviously up-regulated at 12th or 20th weekend while the expression of eNOSmRNA was down-regulated at 20th weekend in diabetes rats. All these abnormalities were partially attenuated by valsartan. Conclusion The abnormal change of the NO and expression of NOSmRNA might be related to the cardiomyopathy in type 2 diabetes. Valsartan might play a protective role in the myocardial disease.

Aim To investigate the effects of anisodamine on the pressure of portal vein of experimental liver fibrosis and its mechanisms of action. Methods The experimental liver fibrosis model was produced by CCl_4. The preventive group was treated ten weeks with anisodamine 7.0 mg?kg~(-1) ip once everyday. All therapeutic groups were treated six weeks with anisodamine 7.0 mg?kg~(-1) or 14.0mg?kg~(-1) ip once everyday. After CCl_4 injection for ten weeks, the pressure of portal vein,the content of NO in livers, and liver iNOS and eNOS mRNA expressions were detected with different methods.Results The pressure of portal vein was significantly reduced in anisodamine preventive group and anisodamine therapeutic groups. The liver content of NO and the expression of iNOS and eNOS were all inhibited by the treatment of anisodamine.Conclusion Anisodamine reduced the expressions of iNOS and eNOS to synthesis of NO in liver. As a result, the pressure of portal vein of fibrosis rats decreased. So Portal hypertension of liver fibrosis may be improved by anisodamine in patients.