Kouzilan was selected as a potent hypotensive drug, and two fractions, K01 (hydrosoluble element) and K02 (fat-soluble element), were extracted from it. Thepresent study focused on its mechanism of vascular effects in vitro. The data showed thatK01 and K02 antagonized the contraction of isolated thoracic aortic ring of SD rat, indu-ced by norepinephrine (NE, 1 ?mol/L). The IC_(50) values of K01 and K02 were 1.98g/Land 1.15g/L respectively, and that of Verapamil (Ver) was 0.88 ?mol/L. K01, K02 andVer all shifted the dose-response curves of NE to the right in a noncompetitive antagonis-tic manner, and they also depressed the maximal efficacy of contraction. Added NE intoa calcium-free K-H solution to induce aortic vessel contraction (phase 1), then added cal-cium (2.5mmol/L) to induce continued contraction (phase 2), K01 depressed phase 2significantly. In lower concentration, K02 was similar to K01, however, in higher concen-tration, it depressed phase 1 and phase. 2 significantly, which was similar to Ver. Theseresults suggested that K01 and K02 had a vasodilative effect, which was related to theblockade of the receptor operated calcium channel (ROC). K02 inhibited both the calciumrelease from intracellar storage sites and the influx of extracellar calcium, but K01 onlyinhibited the latter.

Long Jing 1 (L01) is the effective component extracted from asiatic todd-alia. In the experiments on rat thoracic aortic rings, L01 45-405 ?mol/L inhibited thecontraction initiated by high K~+ or NE, the IC_(50) value was 206.93 and 94.18 ?mol/Lrespectively. L01 shifted the dose-response curve of KCl or NE to the right, and reducedthe maximal response, also shifted that of CaCl_2 to the right parallelly. The effects ofL01 were similar to that of Ver (verapamil) in the blockage on PDC. Morever L01 80 ?mol/Linhibited the release of intracellular Ca~(2+) and extracellular Ca~(2+) influx initiated by NE,the former effect was more significant than the latter (this was different from Ver). Theseresults suggested that L01 was probably a new calcium antagonist different from Ver.

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.

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.

Many snake venoms contain complex mixtures of pharmacologically important molecules, some of which show potential therapeutic value in the treatment of cancer and other human disorders. In this review, we mainly reports the effects of snake venom active components, such as disintegrins and lectins in paralyzing cancer cells, blocking on cell migration, interaction with integrins, inhibition of tumor dissemination and angiogenesis. The advanced researches on the snake venom's apoptosis-inducing components on tumors are also introduced. [

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 explore the effects and mechanism of cobra venom serum on the proliferation in HL60 cells. METHODS Established the HL60 cells as a target to study the growth feature by the action of cobra venom serum.The agarose gel electrophoresis and flow cytometry analysis were used to demonstrate apoptosis. RESULTS Compared with the control group, the cells were inhibited significantly by the action of cobra venom serum.A characteristic DNA "ladder" was detected by using agarose gel electrophoresis. By flow cytometry analysis,it was proved that most apoptosis of HL60 cells occurred when cultured with cobra venom serum. CONCLUSION Cobra venom serum inhibited the HL60 cells in vitro , which was related to apoptosis. This may introduce a new way to the treatment of leukemia.

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 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?.