Objective To explore the pharmacological function of immune enhancer of gypenosides and discuss the dose-effect relationship.Methods The gypenosides was used as an immune enhancer to cure the immune deficit mouse and observe non-specific immunological function by carbon clear test.All of the mice were administrated with CTX and then were divided into six groups:control group,high dose group,middle dose group,lower dose group.Respectively,the carbon clear test was performed in each group and the variation of non-specific immune function was observed.Results The carbon clear test showed that the index of carbon clear test in control group was markedly decreased while the index of carbon clear testing high and middle group was increased.The effect of gypenosides was dose-dependent on the non-specific immune.Conclusion Gypenosides can markedly increase the non-specific immune function.

Mycophenolate acid is a novel immunosuppressive drug. Its target of action is the isomerⅡof inosine 5'-monophosphate dehydrogenase(IMPDH). It inhibits de nove purine synthesis and also decreases expression of adhesive molecule. It inhibits selectively the proliferation of lymphocyte, so that it has strong immunosuppressive effects on various rejections to allograft or xenograft, and on autoimmune diseases, and has the features of higher potency and lower toxicity.

0.05).There were significant differences among group B,group D and group E(P

Mycophenolate acid is a novel immunosuppressive drug. Its target of action is the isomerⅡof inosine 5'-monophosphate dehydrogenase(IMPDH). It inhibits de nove purine synthesis and also decreases expression of adhesive molecule. It inhibits selectively the proliferation of lymphocyte, so that it has strong immunosuppressive effects on various rejections to allograft or xenograft, and on autoimmune diseases, and has the features of higher potency and lower toxicity.[

AIM:To investigate the changes of apelin in blood and myocardium, and the protective mechanisms of ganoderma spores on myocardial ischemia injury induced by isoproterenol in rats. METHODS: The model of myocardial ischemia injury was induced by subcutaneous injection of high dose isoproterenol. Enzyme linked immunosorbent assay (ELISA) was used to measure the apelin contents in blood and myocardium. Semi-quantitative RT-PCR was used to measure the apelin mRNA level in myocardium. Electron microscope was used to observe the pathomorphological changes of myocardium. Ganoderma spores was administered i.g. for 7 weeks. RESULTS: Compared with the normal control group, the apelin contents in blood and myocardium and the apelin mRNA level in myocardium were significantly decreased in the model group (P

Cobra venom factor (CVF), separated from the cobra venoms, is an acidic glucoproteins with anticomplementory activity. The combination of CVF with factor B in the blood produces a stable C3 and C5 converterase resulting in complement depletion by activating complement continually. There are many studies on it, such as inflammation, autoimmune disease, xenotransplantation, anti-tumor, etc. CVF is also an important tool drug for the study of complement role in the pathophysiological development of diseases.

AIM: To observe the effects of toddalia asiatica aqueous extract (Fei Long No 1, F01) on cardiac function and hemodynamics of acute myocardial ischemia in the animal model. METHODS: High positioned double-ligation of the anterior descending left coronary artery induced acute myocardial ischemia in New Zealand rabbits. F01 268 mg/kg were ip into the acute myocardial ischemic model, Cardiac function and hemodynamic measurements were performed before and after ligation and administration of F01. t -test paired was used for statistical analysis. RESULTS: After ligation all indices was reduced significantly except that LVEDP was markedly increased and t-dp/dt max had little change. After administration of F01 changes of most indices were reversed, and returned to or were close to the baseline. 1.5 h after administration of F01 action was more markedly. But the indices of left ventricle work and consumption of oxygen ( HR, TTI and TTI?HR) were reducing continuously. CONCLUSION: F01 markedly decreases ventricle work and consumption of oxygen of acute ischemic myocardium, so that the contractility, diastolic function of myocardium and cardial output are improved. These are the mechanism of protective effect on myocardial ischemia.

Aim To investigate the effects of Guaveno-ic acid (GA)on proliferation,insulin synthesis and secretion in INS-1 cells and their possible mechanism. Methods INS-1 βcells were cultured in vitro.Control group,medium group,model group,drug groups and positive group were set.INS-1 cells were treated with GA (0.3,1 ,3,1 0,30 nmol·L -1 )for 48 h.The cell proliferation was tested by MTT assay.Acid-alco-hol was used to extract the insulin in the cells and the amount of insulin synthesis of INS-1 cells was tested by RIA.5.6,1 6.7 mmol·L -1 glucose was used to chal-lenge INS-1 cells for 1 h to the insulin secretion model (BIS and GSIS)was tested,and the insulin secretion of INS-1 cells was tested via RIA.The mRNA expres-sion of insulin gene,PDX-1 and MafA was tested by q-PCR.Results Compared with medium group,GA could promote the proliferation of INS-1 cells signifi-cantly (P <0.01 )and promote the synthesis of insulin in INS-1 cells significantly (P <0.01 ).GA(0.3 ~30 nmol· L -1 )could promote the BIS,GSIS of INS-1 cells significantly (P <0.05 or P <0.01 ).GA (3,30 nmol·L -1 )could up-regulate the mRNA expression of insulin gene,PDX-1 ,MafA in INS-1 cells signifi-cantly (P <0.01 ).Conclusions GA could signifi-cantly improve the proliferation of INS-1 cells and pro-mote the insulin synthesis and secretion of INS-1 cells, which may be associated with up-regulation of insulin gene,PDX-1 ,MafA mRNA expression.

0.05). However, in the presence of 16.5 mmol/L glucose, PGF_ 2? increased significantly in insulin secretion (P

Aim To investigate whether SC58125 synergized with TNF-? to induce HT-29 cell apoptosis and study the possible molecular mechanism. Methods By using MTT, agarose gel electrophoresis and flow cytometry, we examined the effect of SC58125/TNF-? on cell proliferation and apoptosis in HT-29 cells. The activity of caspase-3 and the changes of I?B? and NF-?B were also measured after treatment with SC58125 by Electrophoretic mobility shift assay and Western blot. Results Both SC58125 and TNF-? exhibited cytotoxicity, the combination of the two agents significantly reduced HT-29 cell viability in a dose-dependent manner. TNF-?-treated cells showed oligonucleosomal cleavage of genomic DNA. SC58125 significantly enhanced the inhibition of cell proliferation and inducement of cell apoptosis of TNF-?,the apoptotic index was increased from 11.2%?1.1% to 53.9%?2.1%. SC58125/TNF-?-induced apoptosis of HT-29 cells was accompanied by the induction of caspases-3. I?B? levels were substantially decreased after treatment with TNF-? and the degradation of I?B? was almost completely inhibited when SC58125 was added in NF-?B was activated in HT-29 cells after treatment with TNF-?, whereas pretreatment of HT-29 cells with SC58125 for 2 h, TNF-?-induced NF-?B DNA binding was profoundly inhibited. Conclusion SC58125 synergizes with TNF-? to inhibit cell growth and induce apoptosis in HT-29 cells, which may be mediated by activating caspases and preventing degradation of I?B?.