AIM:To investigate the protective effect of a new type nerves protectant TQ0701-2,as the derivate of edaravone free radical scavenger,on cerebral ischemia reperfusion injury rat.METHODS:120 male SD rats were randomly divided into sham group,model group,edaravone group(3.0 mg/kg)and TQ0701-2 high-dose group(6.0 mg/kg),middle-dose(3.0 mg/kg)and low-dose group(1.5 mg/kg).Animals in the latter five groups were subjected to transient focal ischemia by the middle cerebral artery occlusion(MCAO)for 2 h before reperfusion,while the sham group wasn't ischemic.The rats were injected with edaravone or TQ0701-2 30 min before ischemic and 0 min,2 h after reperfusion in edaravone and TQ0701-2 groups,sham group and model group were treated with normal saline as well.After 24 h of reperfusion,the infarct ratio,neurological and histological deficient and the changes of pathohistology were evaluated.RESULTS:The infarct ratios and neurological deficit scores in the model group were increased(P

AIM: To study antiasthmatic effect of citral from aqueous extract of fruit of cubeb litsea tree and its mechanism.METHODS: By inducing asthma with Ach-histamine method in guinea pig,cough with ammonia in mice and the output quantity of phenol red from the trachea in mice,the antiasthmatic was observed,preventing cough and eliminating phlegm effect of citral. By measuring the tension of guinea-pig isolated tracheal rings,the both influence of citral was observed on isolated guinea pig tracheal rings and inhibition's effects of citral on contraction induced by Ach.RESULTS: Citral prolonged apparently the incubation period of asthma due to Ach-histamine solution in guinea pig and the coughing incubation period,reduced coughing frequency induced by ammonia in mice,increased excretion of phenol red from the respiratory tract in mice,inhibited the constrictions induced by Ach,and shifted the dose-effect curves of Ach to the right.CONCLUSION: Citral has functions of expelling phlegm,relieving cough and resisting asthma,satisfactory bronchi spasmolysis.

Endothelial dysfunction plays a crucial role in the development of arteriosclerosis (AS). Accumulating evidence suggests that endothelial dysfunction is an initiating event in the etiology of arteriosclerosis. This article reviewed the relationship between endothelial dysfunction and atherosclerosis, and the effects of therapeutic drugs especially statins on endothelial dysfunction.

Aim To investigate effects of Icariin in rats with acute myocardial ischemia induced by isoproterenol(ISO).Methods Icariin(12,6,3 mg?kg-1) was administrated through iv pathway for five days.Myocardial ischemia model of rats was induced by subcutaneous injection(sc) of ISO(30 mg?kg-1 for two days,once a day).The change of Electrocardiogram(ECG) was observed.The levels of lactate dehydrogenase (LDH),superoxide dismutase(SOD), malondialdehyde(MDA) and nitric oxide(NO)in serum were measured.Cardiac indexes(HW/BW and LVW/BW)and cardiac infarction area(IS/V%)were examined.Results Compared with the model group,Icariin(12,6,3 mg?kg-1) could effectively reverse the evident change of T wave and J point induced by isoproterenol,notably decrease the levels of LDH and MDA in the serum, distinctly increase the levels of SOD and NO in the serum(P

Aim To investigate the protective effects of on focal cerebral ischemic-reperfusion(I/R)injury in rats.Methods The model of rat middle cerebral artery occlusion(MCAO)was induced to observe the change of praxiology of rats,infarction percentage,water content,histology of the rat brains.The levels of superoxide dismutase(SOD),malondialdehyde(MDA),reduced glutathione hormone(GSH),Na+,K+-ATPase,Ca2+-ATPase,nitric oxide(NO)were also measured.Results Salidroside at different dosages(24,12,6 mg?kg-1)could obviously decrease cerebral function score,cerebral infarct size and water content,and repair pathological injury of focal cerebral I/R in rats.MDA,LD,NO contents in brain tissue were significantly decreased and activities of GSH,SOD were significantly improved.Na+,K+-ATPase,Ca2+-ATPase at dosages of 24,12 mg?kg-1 were also significantly improved.Conclusion Salidroside had protective effects on injuries of cerebral I/R.

AIM:To study the effect of Exendin-4 on the glucose tolerance and serum glucose level in normal animals. METHODS: The fasting blood glucose concentration was tested at 0,1,2,3,4 h and 2,4 week after the first administration of Exendin-4 (0.1, 0.3, 0.9 g/kg, 4 weeks, qd) in Wistar rats ,taking insulin as positive control. Before intragastric administration 2.5 g/kg glucose, Exendin-4 (0.2, 0.6, 1.8 g/kg) were subcutaneously injected, then the fasting blood glucose concentration was tested at 0.5, 1, 2 h after the glucose loading. After hypodermic administration of Exendin-4 (0.2, 0.6, 1.8 g/kg), half of the mice were subcutaneously administrated 2.5 g/kg glucose 15 min later, and the insulin was tested at the end of the experiment. RESULTS:Exendin-4 could not significantly change the fasting blood glucose concentration at different times. The fasting blood glucose concentration was significantly decreased after glucose loading by administration Exendin-4. Exendin-4 could increase the serum insulin concentration remarkably after glucose loading and could not change much without glucose loading. CONCLUSION: The results suggest that the blood glucose regulation of Exendin-4 was related to the concentration of glucose.

Objective:To investigate the effect of nimodipine liposomes for injection(NOLI)on focal cerebral ischemia/reperfusion(I/R)injury in rats.Methods:Seventy SD rats were divided into NDLI 1.00 mg/kg,NDLI 0.50 mg/kg,NDLI 0.25 mg/kg,nimodipine 1.00mg/kg,solvent 10 mL/kg,sham-operation and ischemic model groups.The model of middle cerelral artery occlusion in rat was replicated.The behavioral scores in rats were assessed in all groups.The infarct volume,brain water content,biochemical indices of brain homogenate and histology were detected.Results:1he NDLI 1.00mg/kg,0.50 mg/kg and 0.25 mg/kg groups could significantly improve the behavior scores in focal cerebral ischemic rats,reduce the volume of cerebral infarction,decrease the brain water content,improve the activities of Na+,K+-ATPase,Ca2+-ATPase,glutathione(GSH)and superoxide dismutazse(SOD)in brain tissues,reduce conteras of malondialdehyde(MDA),lactic acid(LA)and nitric oxide(NO),and improve histo logical injury.Conclusions:NDLI has the protective effect on focal cerebral ischemia/reperfusion injury in rats.

Aim To explore the mechanism of E.coli heat-labile enterotoxin B subunit(LTB)as adjuvant by analysis of cellular proteins interacting with LTB. Methods Whole cell proteins were purified from RAW 264.7 cell after treated with LTB or NaCl 12 h, respectively.The cellular proteins were interacted with LTB and the interacting proteins were purified by pull-down assay and identified by mass spectrography.The LTB interaction proteins were conformed with Western blot and immunofluorescence assay.Results 25 LTB interaction proteins were found,and their interaction network was mapped;four proteins (Jup,Dsp,Ddx5 and Vimentin)were indicated to be related with LTB adjuvant activity;immunofluorescence assay indicated that GM130 interacted with LTB,however,Vimentin had no interaction with LTB in vivo.After treated by LTB,the expression of β-actin was upregulated obvi-ously in RAW 264.7 cell,whereras,Hspd1 did not show any change.Conclusions LTB exerts adjuvant activity through binding to GM1 of immune cells,cau-sing endocytosis and transporting to the Golgi apparatus by vesicles.Then LTB might bind to Jup and affect TCF/LEF activity,regulating the expression of Bcl 2, IL-6,and Runx3.The result is promoted T cell and B cell proliferation,differentiation and activation by se-cretion of cytokines and immunoglobulins.

A series of andrographolide derivatives with the structure of 12-N-substituted-14-deoxyandrographolide were synthesized from the parent compound andrographolide.Their antitumor activities were preliminarily evaluated on various cancer cell lines and compound 4d stood out due to its potent growth inhibitory effect in comparison with andrographolide.Compound 4d also demonstrated significant antitumor effect on human hepatoma HepG2cells in vitro and on sarcoma 180 (S180) and hepatoma 22(H22)-bearing mice in vivo.Then,the apoptosis induced by compound 4d in HepG2cells was detected by Annexin V/PI double staining assay.Further mechanic study showed that the expression of p53 and Bax was significantly elevated and that of Bcl-2was downregulated in 4d-treated HepG2cells.Collectively,these data suggested that compound 4d had remarkable antitumor effect both in vitro and in vivo and could effectively induce apoptosis via a p53-dependent pathway in HepG2 cells,thus deserving further investigation.

Aim Tostudytheeffectsofferulicacid (FA) on doxorubicin (DOX) induced cellular injury inH9c2ratmyocardialcells.Methods H9c2cells were treated with 1μmol·L-1 DOX treated for 24 h to establish a myocardial injury model. 10, 20, 40μmol ·L-1 FA was added 2 h before DOX treatment. Cell viability was measured by cell counter kit ( CCK-8 ) . Morphological changes were observed by phase contrast microscope. LDH, CK, MDA, SOD levels were detec-ted by biochemical kits. Intracellular level of reactive oxygen species ( ROS) was examined by DCF-DA stai-ning with flow cytometry. Cellular apoptosis was detec-ted by AO-EB staining and DNA agarose gel electro-phoresis. The expression of caspase-3, Bax, Bcl-2 was evaluatedbyWesternblot.Results Exposureof H9c2 cells to DOX led to decrease in cell viability, in-crease in stress and apoptosis. FA pre-treatment im-proved cell viability in a dose-dependent manner, at-tenuated leakage of LDH and CK, and reversed mor-phological changes induced by DOX. FA suppressed DOX-induced oxidative stress as evidenced by reducing ROS and MDA generation and increasing SOD enzyme activity. FA depressed myocardial apoptosis by down-regulating pro-apoptotic protein caspase-3 and Bax, whereas up-regulating apoptosis inhibitory protein Bcl-2.Conclusions FAhasaprotectiveeffectonDOX-induced injury in H9c2 cells. This protection may re-sult from inhibition of myocardial oxidative stress and apoptosis.