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 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 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 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.

AIM: To investigate antitumor effect of allotri-tridecyl diethylamine (D-108) in vivo and in vitro. METHODS: The cytotoxic effects of D-108 on various tumor cell lines, human gingival fibroblast and marrow stromal cell cultured in vitro were determined with trypan blue dye exclusion test and MTT method. The acute toxicity of mice by administration of D-108 was evaluated by Bliss method. At a tolerable dose level, D-108 was administrated to treat transplanted solid tumor U14, and tumor weight inhibition was observed. Apoptosis morphological transformation of HL 60 cell induced by D-108 was detected by the Giemsa staining. RESULTS: The cytotoxic effects in vitro of D-108 on various tumor cell lines (IC_ 50 : 0.22 to 2.19 mg?L~ -1 ) were more powerful than both human gingival fibroblast and marrow stromal cell (IC_ 50 : 5.55 and 3.57 mg?L~ -1 ). LD_ 50 of D-108 was 36.49 mg?kg~ -1 (mice, i.g.). D-108 inhibited in vivo growth of implanted solid tumor U14 of mice effectually. The inhibition rate of tumor weight of D-108 (100 mg?kg~ -1 ?d~ -1 i.g.) was 45.27 %. HL 60 cell appearanced typical apoptosis morphological transformation induced by D-108. CONCLUSION: D-108 had obvious antitumor activity in vivo and in vitro and little toxicity. D-108 could induce the apoptosis of HL 60 cell.

AIM: To study the protective effects of nimodipine liposomes for injection (NDLI) on injuries of total cerebral ischemia/reperfusion(I/R) in rats and anoxia in mice. METHODS: Acute anoxia in mice was produced by hypoxia under normal pressure and decapitation. In these two models the survival time and persistent time of gasping were observed. Ameliorated pulsinelli four-vessel occlusion method was used to make global brain ischemia model. The EEG, the time of righting reflex recovery and Evans blue content in the homogenate of the brain tissues were recorded. RESULTS: NDLI obviously prolonged the survival time and persistent time of gasping in mice subjected to acute anoxia, remarkably shortened the time of EEG recovery and righting reflex recovery, and reduced Evens blue content in the homogenate. CONCLUSION: NDLI has significantly protective effects on injuries of total cerebral I/R and anoxia.

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.

Objective To observe the effects of ginkgolides on hypoxia tolerance in mice and on myocardial ischemia injury in rats.Methods The mice were given isoprenaline 20 mg/kg(ip) and the survival time of the mice model under the hypoxic condition was recorded. Rat myocardial ischemia was induced by subcutaneous injection of over- dosage isoprenaline(8 mg/kg). Before modeling, rats were pretreated with ginkgolides 10, 20, 40 mg/kg, of ginkgo biloba( EGb) Extract 300 mg/kg, Propranolol 5 mg/kg,or vehicle for four days. The histological changes of myocardiim, serum creatine phosphokinase (CPK) level and lactate dehydrogenase (LDH) activity, myocardial lactate dehydrogenase(LDH) and superoxide dismutase (SOD) content were detected.Results Ginkgolides could prolong the survival time in the mice under a hypoxic condition, lessen the isoprenaline- induced rat myocardial ischemia, inhibit the activities of serum CPK and LDH and the increase of MDA content in ischemic myocardial tissue, enhance superoxide dismutase (SOD) activity. Conclusion Ginkgolides enhance to hypoxia the tolerance in mice and prevent rats from myocardial ischemic injury. The protective mechanism may be related to its inhibition of the activity of platelet activating factor and oxygen free radical. 

Objective To observe the effects of total flavones from Herba Epimedii(TFHE)on the experimental myocardial ischemia and hemorheology of animals.Methods The model of acute myocardial ischemia of rats was established with pituitrin and the model of acute blood stasis was established with high-molecular dextran.The effects of TFHE on the electrocardiogram J-point of acute myocardial ischemia model and the hemorheology of acute blood stasis model were observed.Besides these,the effects of TFHE on coaglutaion time in mice were observed.Results As compared with the model groups,high-,middle-,and low-dosage groups(24,12,and 6 mg/kg)of TFHE could obviously improve the abnormal electrocardiogram J-point of acute myocardial ischemia model,also could effectively prevent the ascending of whole blood viscosity(high-,middle-,and low-shear rate),packed erythrocyte volume,and fibrinogen.High-and low-dosage groups(34 and 17 mg/kg)of TFHE could obviously lengthen the coaglutaion time in mice.Conclusion The results suggest that TFHE possesses protective effects on ischemic myocardium,which may better hemorheology,decrease the whole blood viscosity,prevent blood from coagulating and improve the circulatation of coronary artery.