Alveolar echinococcosis (AE) is a potentially fatal zoonosis caused by Echinococcus multilocularis (E .m) , primary located in the liver and showed malignant invasion .AE can develop to the lungs and brain metastases .Operation treat-ment and medication therapeutic efficacy show poor effect .The mechanism of AE invasive growth and metastasis is unclear . Angiogenesis is a highly regulated behavior in normal tissues .Abnormal angiogenesis is one of the key signs of malignant tumor ,and VEGF is one of the key mediators of angiogenesis .Numerous studies have shown that VEGF and CD34 plays an important role in the formation of tumor angiogenesis and invasive growth process .This article discussed the role of angiogene-sis in AE aggressive ,aimed to provide a new way for the clinic conservative treatment for patients with advanced stage ,preven-ting recurrence after operation ,and adjunctive therapy of operation and drug .

Objective To observe the clinical efficacy ofXiaozhikang Formula Granules for the treatment of nonalcoholic fatty liver disease.Methods Totally 90 patients with nonalcoholic fatty liver disease were randomly divided into control group and treatment group, 45 cases in each group. Patients in the control group were treated with conventional western treatment and oral metformin enteric-coated metformin hydrochloride, while patients in the treatment group were treated withXiaozhikang Formula Granules on the basis of conventional western treatment for 3 months. Blood lipid and insulin resistance in the two groups before and after treatment were observed, and the clinical efficacy between the two groups was compared.Results Clinical excellence (35.5%), total effective rate (84.5%) and TCM syndrome score (13.78 ± 3.6) after treatment of treatment group were better than those of control group (P<0.05). GPT, GOT, TG, and TC in both groups were lower after the treatment (P<0.05,P<0.01). There existed statistical significance in TC and TG between the two groups after treatment (P<0.05). There existed statistical significance in B ultrasound index between the two groups after treatment (P<0.05), and the treatment group was superior. FBG and HOMA-IR in both groups significantly decreased after treatment (P<0.05), and the FBG in the treatment group after treatment was better than control group (P<0.05).Conclusion The efficacy ofXiaozhikang Formula Granules in the treatment of nonalcoholic fatty liver disease is remarkable.

Objective To study the protective mechanism of Gross Saponin Tribulus Terrestris(GSTT) on the neonatal rat ventricular cardiocytes injured by hypoxia and the effect on protein kinase C(PKC).Methods The hypoxia-ischemia model was performed by treating the cultured neonatal rat ventricular cardiocytes with NaCN.The effect of GSTT(100 and 30 mg?L~(-1)) on the contents of ?PKC and ?PKC were detected by flow cytometry and laser confocal microscopy system.Results GSTT up-regulated ?PKC and ?PKC expressions.The contents of ?PKC and ?PKC in GSTT 100 mg?L~(-1) group(1 325.00?53.25,810.55?36.89;66.22?6.23,40.12?2.21) were increased significantly than those in model group(792.00?32.36,492.40?30.15;32.70?2.78,29.28?4.82)(P

Aim To observe the protection effect of Tribulus terrestris saponin monomer B (TTSMB) on cadiocytes impaired by hypoxia-reoxygenation (H/R).Methods Cadiocytes of neonate rat were cultivated for 72 hours and divided into normal control group, H/R group,GSTT 100 mg·L~(-1) group and TTSMB 10,1,0.1 nmol·L~(-1) group.Morphocytology change of cadiocytes was observed after the treatment.Cadiocyte survival rate was detected with MTT colorimetric method.Levels of creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), malondialdehyde (MDA), and activity of superoxide dismutase (SOD) were determined. Apoptosis rate was detected with flow cytometry.Expression of caspase-3 was examined with western blot.Results Compared with the control group, the survival cell number in H/R group decreased obviously, content of CK,LDH, AST, MAD increased, and activity of SOD decreased (P<0.01).Compared with the model group, the survival cell population increased in TTSMB 10,1,0.1 nmol·L~(-1) group (P<0.05 and P<0.01).Contents of CK, LDH, AST, MAD decreased, whereas the activity of SOD increased (P<0.05 and P<0.01).Apoptosis rate and expression of caspase-3 also reduced in TTSMB 10,1,0.1 nmol·L~(-1) group.Conclusion TTSMB has significant cadiocytes protective effect against H/R and inhibits cadiocyte apoptosis,and the mechanism depends on the effect against oxygen free radical.

Fatty acid composition and content in seed oil of plants in Chungbaishan region was studi ed by gas chromatography and reported.

Objective To investigate the effects of angiotensin Ⅰ-converting enzyme inhibitor Enalaprilat(Ena) on proliferation and nitric oxide synthase-nitric oxide system of neonatal rat cardiac fibroblasts(CFb)and to probe its anticardiac fibrosis mechanism.Methods The cultured neonatal Wistar rat CFb were divided into control group,model group and three doses of Ena groups.CFb were isolated by trypsin digestion method.MTT colorimetric assay was adopted to evaluate cell proliferation,flow cytometry was used to measure cell cycle,nitric acid reductase method and spectrophotometry were used to detect the NO contents and NOS activity respectively with Ena.Results Ena could inhibit CFb proliferation induced by AngⅡ,there were significant differences of MTT values between model group and Ena groups after treated for 24,48 and 72 h(P

Objective To investigate the effect of taurine(Tau) on the myocardial fibrosis and its mechanism.Methods The rat model of myocardial fibrosis was built by subcutaneous injection of isoprel(Iso).And the rats were divided into control group,model group and taurine group(80,160,320 mg?kg-1?d-1).Hydroxyproline measurment was carried out for detecting collagen quantification in myocardium tissue.Histopathology changes were detected by HE staining.In vitro,the cultured neonatal rat cardiac fibroblasts(CFb) were divided into control group,model group and taurine group(40,80,160mmol?L-1).The proliferation of CFb was induced by angiotensin Ⅱ(AngⅡ) and detected by the thiazoleblue(MTT)colorimetric assay.TGF-?1 level was determined by ELISA technique.The expression of cyclin dependent kinase inhibitor p27 was assessed with flow cytometry.Results In vivo,the contents of hydroxyproline were decreased in Tau(160,320 mg?kg-1?d-1) groups as compared with model group(P

AIM To investigate the effect of urapidil on NO, ET, ANF and AngⅡ of spontaneously hypertensive rats. METHODS The content of nitric oxide (NO), endothelin (ET), atrial natriuretic factor (ANF) and angiotensin Ⅱ (AngⅡ) were determined by spectrophotometry and radioimmunoassay of spontaneously hypertensive rat (SHR) during the process of decreasing blood pressure with urapidil. RESULTS\ They were as follows: compared with the same aged normal blood pressure WKY rats, in the SHR, the content of serum NO decreased, the level of ET and ANF in the plasma increased. Whereas the level of AngⅡ has no difference in any group. Compared with the control of SHR,urapidil can increase the contents of serum NO, decrease the level of ET and ANF in the plasma. CONCLUSION \ It is suggested that urapidil may adjust the imbalance of cardiovasco-active substances by increasing the release of endogenous vasodilators and reducing the release of endogenous vasocontrictors to antihypertention.

Aim To observe the protective effects of total saponi ns of tribulus (TST) on cerebral ischemia reperfusion injury in rats. Meth ods Rat cerebral ischemia-reperfusion injury was induced by middle cer ebral artery occlusion .The neurological outcome was evaluated. CK, LDH and NO a ctivity in serum,SOD and MDA levels of cerebral tissue were measured. Re sults The levels of CK,LDH,NO,SOD and MDA in TST(30 mg?kg -1,1 0 mg?kg -1) groups were significantly lower than those in model group. The level of cellular and intercellular edema was reduced markly in the pathomorpho logy examination. The neurological deficits was decreased by TST.Conclus ion TST has protective effects on cerebral ischemia reperfusion injur y in rats.