1.Review on endothelial dysfunction in atherosclerosis and drug therapy
Zheyi HU ; Qiujuan WANG ; Xuansheng DING
Chinese Journal of Clinical Pharmacology and Therapeutics 2002;0(05):-
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.
2.Empirical study on antiasthmatic effect of citral from aqueous extract of fruit of cubeb litsea tree
Zhiyong YIN ; Qiujuan WANG ; Ying JA
Chinese Journal of Clinical Pharmacology and Therapeutics 2000;0(02):-
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.
3.Protective effect of TQ0701-2 on cerebral ischemia reperfusion injury in rats
Qian LI ; Qiujuan WANG ; Qinglong GUO
Chinese Journal of Clinical Pharmacology and Therapeutics 2000;0(01):-
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
4.Effects of Icariin on acute myocardial ischemia induced by isoproterenol in rats
Zhiwei PAN ; Qiujuan WANG ; Juan YANG ; Lingyi KONG ; Bei WANG
Chinese Pharmacological Bulletin 1986;0(05):-
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
5.Synthesis and antitumor effect of novel andrographolide derivatives
Qianqian FAN ; Qiujuan WANG ; Bubing ZENG ; Yulin WU ; Hui JI
Journal of China Pharmaceutical University 2010;41(4):326-332
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.
6.Study on antitumor activity of allotri-tridecyl diethylamine in vitro and in vitro
Ruixing WANG ; Xunru HUANG ; Zhijuan WU ; Jing LIN ; Qiujuan FANG
Chinese Journal of Clinical Pharmacology and Therapeutics 2004;0(11):-
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.
7.Protective effects of nimodipine liposomes for injection on injuries of total cerebral ischemia/reperfusion in rats and anoxia in mice
Juan YANG ; Qiujuan WANG ; Zhiwei PAN ; Jiabi ZHU
Chinese Journal of Clinical Pharmacology and Therapeutics 2004;0(12):-
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.
8.Effect of Ginkgolides on Myocardial Ischemic Injury Induced by Isoprenaline
Jian GAO ; Qiujuan WANG ; Yu TANG ; Yuhang LI
Traditional Chinese Drug Research & Clinical Pharmacology 1993;0(03):-
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.
9.Effects of total flavones from Herba Epimedii on experimental myocardial ischemia and hemorheology of animals
Qiujuan WANG ; Zhiwei PAN ; Pan YUE ; Lingyi KONG
Chinese Traditional and Herbal Drugs 1994;0(07):-
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.
10.Effect of Exendin-4 on the glucose tolerance and serum glucose level in normal animals
Lin YUAN ; Tianhua YAN ; Qiujuan WANG ; Qinglong GUO
Chinese Journal of Clinical Pharmacology and Therapeutics 2000;0(03):-
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.