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Frequent ventricular premature beats increase blood pressure variability in rats

Acta Pharmacologica Sinica 2004年第5期25卷 3-11页

作者： Chao-yu MIAO2. Li-ping XU, Jian-guo LIU, He-hui XIE, Wen-jun YUAN, Ding-feng SU2.epartment of pharmacology, Second Military Medical {3., Shanghai 2.043.,{2. Department of pharmacology Second Military Medical University

AIM: The present study was designed to test a hypothesis that nonfatal ventricular arrhythmia such as ventricularpremature beats (VPB) is a contributing factor in the elevation of blood pressure variability (BPV). METHODS:Blood pressure (BP) and electrocardiogram were continuously recorded. The relation between VPB and BPV wasobserved under conscious state in chronic myocardial infarction (MI) rats one month after ligation of the leftcoronary artery, and further verified under anesthetized state in rat model of ventricular arrhythmia produced byacute intravenous infusion of aconitine. RESULTS: MI rats exhibited a big difference in the count and pattern ofVPB, and were divided into no VPB, occasional VPB, and frequent VPB groups. Among the three groups, therewere no differences in BP, heart period (HP), and MI size. However, BPV was markedly higher in frequent notoccasional VPB rats, and HP variability (HPV) was larger in both frequent and occasional VPB rats, when comparedwith no VPB rats. In the whole population of MI rats, BPV was positively correlated with VPB and HPV, not withBP, HP and MI size. Infusion of aconitine had no effect on BP, HP, BPV, and HPV during the period without *** VPB after several minutes of aconitine infusion induced significant increase in BPV and HPV with nochange in BP and HP. BPV was also positively correlated with VPB and HPV, not with BP and HP. Hemodynamicsin aconitine-evoked ventricular tachycardia was characterized as lower BP, higher BPV, and higher ***: High BPV can be caused by frequent not occasional VPB in rats.

关键词： arrhythmia blood pressure variability heart period variability

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Binding of PLCδ1PH-GFP to Ptdlns(4,5)P2.prevents inhibition of phospholipase C-mediated hydrolysis of Ptdlns(4,5)P2.by neomycin

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Acta Pharmacologica Sinica 2005年第12期26卷 1485-1491页

作者： Chuan WANG Xiao-na DU Qing-zhong JIA Hai-lin ZHANG~2.Department of pharmacology Hebei Medical university,Shijiazhuang 050017,{2. Department of pharmacology Hebei Medical University Shijiazhuang China

Aim:To investigate the effects of the pleckstrin homology(PH)domain of phos-pholipase Cδ1(PLCδ1PH)on inhibition of phospholipase C(PLC)-mediated hy-drolysis of phosphatidylinositol 4,5-bisphosphate[PtdIns(4,5)P2.by ***:A fusion construct of green fluorescent protein(GFP)and PLCδ1PH(PLCδ1PH-GFP),which is known to bind PtdIns(4,5)P2.pecifically,together withlaser-scanning confocal microscopy,was used to trace PtdIns(4,5)***:Stimulation of the type 1 muscarinic receptor and the bradykinin 2.recep-tor induced a reversible PLCδ1PH-GFP translocation from the membrane to thecytosol in COS-7 *** inhibitor U73.2. blocked the ***,a known PtdIns kinase inhibitor,did not affect the translocationinduced by ACh,but blocked recovery after translocation,indicating thatPtdIns(4,5)P2.ydrolysis occurs through receptor-mediated PLC ***,a commonly used phospholipase C blocker,failed to block the recep-tor-induced PLCδ1PH-GFP translocation,indicating that neomycin is unable toblock PLC-mediated Ptdlns(4,5)Pe ***,in the absence of PLCδ1PH-GFP expression,neomycin abolished the receptor-induced hydrolysis ofPtdIns(4,5)P2.by ***:Although PLCδ1PH and neomycin bind toPtdIns(4,5)P2.in a similar way,they have distinct effects on receptor-mediatedactivation of PLC and PtdIns(4,5)P2.hydrolysis.

关键词： phosphatidylinositol 4,5-bisphosphate neomycin phospholipase C pleckstrin homology domains competitive binding acetylcholine green fluorescent proteins

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Doxepin protects cultured neurons against oxidative stress-induced injury

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Acta Pharmacologica Sinica 2004年第3期25卷 43-46页

作者： Bian-sheng JI,He JI1,Guo-qing LIU2.Department of pharmacology,china Pharmaceutical {2.,Nanjing 2.0009 1Department of Medicine,Henan {2.,Kaifeng 475001,china Department of pharmacology China Pharmaceutical University Department of Medicine Henan University

AIM: To investigate protective effects of doxepin (Dox) on cultured neuronal injury induced by oxidative stress. METHODS: Cytotoxicities of glutamate (Glu 0.5 mmol/L, 15 min), sodium dithionite (0.5 mmol/L, 2. h) or hemo- globin (Hb100 mg/L,2. h)and the protective effects of Dox were observed. RESULTS: Exposure of cultured neurons to Glu, sodium dithionite and Hb developed a neurotoxicity expressed in the thiazol blue tetrazolium bro- mide (MTT) assay, the increase of lactate dehydrogenase (LDH) leakage, malondialdehyde (MDA) content and intracellular [Ca2.]i accumulation, as well as the decrease of superoxide dismutase (SOD) activity. DOX 1-100 nmol/L significantly inhibited all above changes. CONCLUSION: Dox protects cultured neurons against oxidative stress-induced injury by suppressing intracellular [Ca2.]iaccumulation, decreasing lipid peroxide generation and stimulating antioxidant enzyme.

关键词： doxepin ischemia glutamic acid hemoglobins neurons

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CYP2.1 mediated isoniazid-induced hepatotoxicity in rats

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Acta Pharmacologica Sinica 2004年第5期25卷 157-162页

作者： Jiang YUE, Ren-xiu PENG1, Jing YANG, Rui KONG, Juan LIUDepartment of pharmacology, Medical College of wuhan {2., wuhan 43.071, china Department of pharmacology Medical College of Wuhan University

AIM: To investigate the role of CYP2.1 in isoniazid (INH)-induced hepatotoxicity and the influence of rifampicin(RFP) on INH-induced liver injury. METHODS: Rats were treated with INH alone (100 mg/kg, ip) or co-administeredwith RFP (100 mg/kg, ig) for 10 d and 2. d. Hepatotoxicity was assayed by plasma enzymes (sALT, sAST) andhistopathological examinations. Hepatic CYP2.1 activity was measured by aniline hydroxylase (ANH), and CYP2.1mRNA expression was determined by RT-PCR. Plasma hydrazine concentration was determined by ***: For a 10 d INH-treatment, hepatic CYP2.1 level was increased to 3.7-fold over the control; liverimpairment appeared after 2. d treatment, while CYP2.1 and plasma hydrazine were, respectively, increased to 4.6-fold and 1.7-fold. However, in INH-RFP group for 10 d, CYP2.1 and plasma hydrazine were, respectively,decreased by 13.% and 18 % over INH group; similarly, hepatic injury is equal to INH group appeared after 2. d,and CYP2.1 was further decreased by 2. %. Correlation analysis showed that sALT had a positive correlation withplasma hydrazine and with CYP2.1 activity; CYP2.1 activity was also markedly correlated with plasma *** compared with control, there is no difference in changes of CYP2.1 mRNA expression in INH and INH-RFPtreatment for 2. d. CONCLUSION: The metabolite of INH, hydrazine, plays an important role in INH-inducedhepatotoxicity in rats. The induction of CYP2.1 by hydrazine is involved in the hepatotoxicity of INH. RFP doesnot exacerbate INH-induced hepatotoxicity in short term, which relates to down-regulation of CYP2.1.

关键词： isoniazid rifampin hydrazines cytochrome P-450 CYP2.1

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Effects of esculentoside A on production of interleukin-1, 2. and prostaglandin E2

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Acta Pharmacologica Sinica 2004年第6期25卷 115-119页

作者： Zhen-yu XIAO, Qin-yue ZHENG, Yuan-ying JIANG, Bin ZHOU, Ming YIN2. Hong-bin WANG, Jun-ping ZHANG3. Department of pharmacology,Second Military Medical university, Shanghai2.043. 2.ollege of Pharmacy,Jiao Tong university, Shanghai 2.003., china Department of pharmacology Second Military Medical University Shanghai 200433 China

AIM: To investigate the influence of esculentoside A (EsA) on immunological function and its mechanism of anti- inflammation. METHODS: Interleukin-1 production was measured by thymocyte co-stimulating assay; the radio- activity of [3.]arachidonic acid (AA) was used to evaluate the release of AA; prostaglandin E2.production was measured with radioimmunoassay (RIA); IL-2.and IFN-γ were detected by ELISA method. RESULTS: EsA (3.12. μmol/L)could potently inhibit the production of IL-1 and PGE2.from both silent and LPS induced macrophages. EsA had no significant effect on the release of AA from murine macrophages. EsA could inhibit the production of IL-2.from murine lymphocytes induced by ConA, but not affect the production from silent lymphocytes. EsA showed no effect on the production of IFN-γ from both silent and ConA induced lymphocytes. CONCLUSION: EsA could affect the immunological function through inhibiting the production of IL-2.from activated splenocytes and the inhibition of production of IL-1 and PGE2.might be one of the anti-inflammation mechanisms of EsA.

关键词： esculentoside A interleukin-1 interleukin-2 prostaglandins E interferon-gamma

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Traditional Chinese medicine in treatment of opiate addiction

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Acta Pharmacologica Sinica 2006年第10期27卷 1303-1308页

作者： Jie SHI~2.Yan-li LIU~3.Yu-xia FANG~4 Guo-zhu XU~2.Hai-fen ZHAI~2.Lin LU~(2.5,6) ~2.ational Institute on Drug Dependence,Peking university,Beijing 100083.china ~3.ollege of Pharmacy,Soochow university,Suzhou 2.512.,china ~4Clinical pharmacology and Therapeutics Branch,Intramural Research Program.National Institute on Drug Abuse,National Institutes of Health,Baltimore,Maryland 2.2.4,USA.5Behavioral Neuroscience Branch,Intramural Research Program,National Institute on Drug Abuse,National Institutes of Health,Baltimore,Maryland 2.2.4,USA National Institute on Drug Dependence Peking University Beijing 100083 China. linlu@***.

Traditional Chinese medicine (TCM) includes Chinese medicine and *** medicine consists of natural products including plants,animals *** has been practiced in china for more than 2.00 years,and for thepast 2.0 years has been used in treatment of drug *** Chinese medi-cines for the treatment of opiate addiction have been approved by the ChineseState Food and Drug Administration (SFDA),and at least 6 are in clinical *** general therapeutic principle of Chinese medicine developed was based on itsunique theory of"reinforcing healthy Qi and resolving and removing effects oftoxicity".Acupuncture,another essential part of TCM,which was developedbased on the principle that"functions of the human body are controlled by the‘Jing-Luo’and‘Qi-Xue’system",has been used not only in china,but also inEurope,the USA and other countries,for controlling opiate *** aresome advantages in using TCM for opiate detoxification,including less harmfulside effects,high safety and ideal effects in the inhibition of protracted with-drawal symptoms and ***-administration of TCM with modern medicineshows some synergistic effects in *** TCM for detoxificationalso have efficacy in the rehabilitation of abnormal body functions induced bychronic drug use,including improving immune function,increasing working memoryand preventing neurological *** that TCM is effective in the preven-tion of relapse and causes fewer side effects,it may be used widely in the treat-ment of opiate addiction.

关键词： Chinese medicine acupuncture opiate addiction withdrawal relapse treatment

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Establishment of liver specific glucokinase gene knockout mice: a new animal model for screening anti-diabetic drugs

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Acta Pharmacologica Sinica 2004年第12期25卷 93-99页

作者： Ya-li ZHANG, Xiao-hong TAN2. Mei-fang XIAO, Hui LI, Yi-qing Mao, Xiao YANG2. Huan-ran TAN3. Department of pharmacology, School of Basic Medical Science, Peking {3. Health Science Center, Beijing 100083.2.nstitute of Biotechnology Academy ofMilitary Medical Science, Beijing 100071,{2. Department of pharmacology School of Basic Medical Science Peking University Health Science Center Beijing 100083 China

AIM: To characterize the liver-specific role of glucokinase in maintaining glucose homeostasis and to create an animal model for diabetes. METHODS: We performed hepatocyte-specific gene knockout of glucokinase in mice using Cre-loxP gene targeting strategy. First, two directly repeated loxP sequences were inserted to flank the exon 9 and exon 10 of glucokinase in genomic DNA. To achieve this, linearized targeting vector was electroporated into ES cells. Then G418- and Gancyclovir-double-resistant clones were picked and screened by PCR analysis and the positives identified by PCR were confirmed by Southern blot. A targeted clone was selected for microinjection into C57BL/6J blastocysts and implanted into pseudopregnant FVB recipient. Chimeric mice and their offspring were analyzed by Southern blot. Then by intercrossing the Alb-Cre transgenic mice with mice containing a conditional gk allele, we obtained mice with liver-specific glucokinase gene knockout. RESULTS: Among 161 double resistant clones 4 were positive to PCR and Southern blot and only one was used for further experiments. Eventually we generated the liver specific glucokinase knockout mice. These mice showed increased glucose level with age and at the age of 6 weeks fasting blood glucose level was significantly higher than control and they also displayed impaired glucose tolerance. CONCLUSION: Our studies indicate that hepatic glucokinase plays an important role in glucose homeostasis and its deficiencies contribute to the development of diabetes. The liver glucokinase knock- out mouse is an ideal animal model for MODY2. and it also can be applied for screening anti-diabetic drugs.

关键词： animal disease model non insulin dependent diabetes mellitus type 2.diabetes mellitus glucokinase knockout mice

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Acetazolamide inhibits aquaporin-1 protein expression and angiogenesis

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Acta Pharmacologica Sinica 2004年第6期25卷 110-114页

作者： Yang XIANG2. Bing MA, Tao LI, Jun-wei GAO, He-ming YU3. Xue-jun LI4 Departmentof pharmacology, School of Basic Medical Sciences, Peking university, Beijing 100083.2.ife Science Institute, Nanjing university, Nanjing 2.0093.3.ational Research Institute for Family Planning, Beijing 100081,china Department of pharmacology School of Basic Medical Sciences Peking University Beijing 100083 China

AIM: To study effects of acetazolamide on aquaporin-1 (AQP1) protein expression and angiogenesis. METHODS: Establishing Lewis-lung-carcinoma model, the localization of AQP1 in tumor tissues was investigated by immuno- histochemical methods; The biological activity of acetazolamide was detected by endothelial cells proliferation test (MTT) assay and chorioallantoic membrane (CAM) vascular inhibition test. RESULTS: Immunohistochemical localization of AQP1in mice tumor was labeled in capillaries, post capillary venules endothelial cells. After being treated with acetazolamide, the number of capillaries and post capillary venules was significantly decreased in tumor tissue. Acetazolamide showed significant inhibitory effect on angiogenesis in CAMand endothelial cell proliferation. CONCLUSION: Acetazolamide might be identified and developed as one of potential lead compounds for a new therapeutic intervention in inhibiting cancer angiogenesis.

关键词： neoplasms acetazolamide angiogenesis inhibitors CHIP2.

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Inhibition of platelet aggregation by polyaspartoyl L-arginine and its mechanism

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Acta Pharmacologica Sinica 2004年第4期25卷 71-75页

作者： Yin-ye WANG, Zhi-yu TANG, Min DONG, Xiao-yan LIU, Shi-qi PENG2.Department of pharmacology, Department of Medicinal Chemistry, 2.Schoolof Pharmaceutical Sciences, Peking {3., Beijing 100083.{2. Department of pharmacology Department of Medicinal Chemistry School of Pharmaceutical Sciences Peking University

AIM: To observe the oral anti-platelet efficacy and the potential action mechanism of polyaspartoyl L-arginine (PDR), a new L-arginine rich compound. METHODS: Platelet aggregation was conducted by Born’s method; bleeding time was determined using tail’s bleeding time in mice; platelet adhesion was carried out with glass bottle method; nitric oxide (NO) was tested with Griess’ method; and cAMP, thromboxane B2.(TXB2. and 6-keto-PGF1α were assessed with commercial kits. RESULTS: The inhibition by PDR (15-60 mg/kg ig or 10 mg/kg iv) of platelet aggregation induced by adenosine diphosphate (ADP), collagen or thrombin at 1 h after oral administration or at 2. min after iv injection for rats (P3. mg/kg) increased NO concentration in plasma. On the other hand PDR did not change the contents of cAMP in platelet and TXB2.or 6-keto-PGF1α in plasma. CONCLUSION: PDR is a novel, oral effective platelet aggregation inhibitor and its action mechanism possibly related to increasing NO generation.

关键词： platelet aggregation bleeding time platelet adhesiveness polyaspartoyl L-arginine nitric oxide cyclic AMP Thromboxane B2 6-ketoprostaglandin F1 alpha

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Bradykinin potentiates 5-HT3.receptor-mediated current in rat trigeminal ganglion neurons

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Acta Pharmacologica Sinica 2005年第4期26卷 428-434页

作者： Wang-ping HU~(1,2. Xue-mei LI~2.Ji-liang WU~3.Min ZHENG~3.Zhi-wang LI~4 2.Department of Physiology,3.Department of {3.,Xianning College,Xianning 43.100,china 4 Department of Neurobiology,Tongji Medical College of {2. university of Science and Technology,wuhan 43.03.,china DepartmentofPhysiology XianningCollegeXianning437100China

Aim:To explore the modulatory effect of bradykinin （BK） on 5-HT3.eceptor-mediated current in trigeminal ganglion （TG） neurons in ***:The whole-cell patch-clamp technique was used to record 5-HT-activated currents (I5-HT) inneurons freshly dissociated from rat *** were applied by rapid ***:The majority of the neurons examined responded to 5-HTapplied externally with an inward current （76.3.,74/97） that could be blocked bythe 5-HT3.eceptor antagonist,ICS-2.5,93. (1×10-6mol/L).In 66 of the 74 cellssensitive to 5-HT （89.2.）,pretreatment for 3. s with BK (1×10-6-1×10-10mol/L)could potentiate I5-HTwith the maximal modulatory effect occurring at10-7mol/L BK （71.6%+4.9%）.BK shifted the 5-HT concentration-response curveupwards with an increase of 68.9%±7.2. in the maximal current response,but withno significant change in the EC50value （19.1±3.2.μmol/L vs 2..9±3.5 μmol/L;t-test,P>0.05;n=8）.BK potentiated I5-HTin a holding potential-independent manner anddid not alter the reverse potential of *** BK-induced potentiation ofI5-HTwas almost completely blocked by Hoe 140 (5×10-7mol/L),a selective B2.Kreceptor antagonist,and was removed after intracellular dialysis of GF-1092.3.（2.μmol/L）,a selective protein kinase C （PKC） inhibitor,with the re-patch ***:Pre-application of BK exerts an enhancing effect on I5-HTvia a PKC-dependent pathway in rat TG neurons,which may explain the peripheral'mecha-nism of pain and hyperalgesia caused by,for example,tissue damage andinflammation.

关键词： bradykinin 5-HT3.serotonin receptor regulation patch-clamp techniques trigeminal ganglion

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