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TOXICITY AND PHARMACOLOGIC STUDY OF DOXYCYCLINE

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CHINESE MEDICAL JOURNAL 1974年第3期87卷

作者： department of pharmacology Szechwan Medical College Chengtu

EXPERIMENTAL STUDIES ON PREVENTION OF MUSCULAR CRAMPS INDUCED BY TWO F-TYPE SCHISTOSOMICIDES

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CHINESE MEDICAL JOURNAL 1974年第1期87卷

作者： department of pharmacology Shanghai First Medical College Shanghai

15甲基前列腺素 F2α和13去氢ω—乙基前列腺素 F2α对妊娠大鼠血中孕酮的影响

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生理学报 1978年第2期 135-142页

作者： department of pharmacology FIRST MEDICAL COLLEGE OF SHANGHAI 上海第一医学院药理学教研组

15-甲-PGF2α和13-去氢-ω 乙-PGF2α在相同剂量时均能使妊娠7天的大鼠血浆孕酮浓度下降。15-甲-PGFα2组于用药后4、8和24小时血浆孕酮浓度下降,分别为用药前的56.6%、43.7%和13.3%。在给药后72小时所有动物子宫中胚胎已被吸收。13-去... 详细信息

15-甲-PGF2α和13-去氢-ω 乙-PGF2α在相同剂量时均能使妊娠7天的大鼠血浆孕酮浓度下降。15-甲-PGFα2组于用药后4、8和24小时血浆孕酮浓度下降,分别为用药前的56.6%、43.7%和13.3%。在给药后72小时所有动物子宫中胚胎已被吸收。13-去氢ω-乙-PGF2α组于用药后4、8和24小时血浆孕酮浓度分别为用药前的63.5%、34.4%和51.9%,给药后72小时大多数动物子宫中仍有胚胎,但胚胎比对照组显著为小,且多游离于子宫中。在给15-甲-PGF2α前30分钟和第二次给15-甲-PGF2α的同时,肌注 HOG 20国际单位,能完全对抗15-甲-PGF2α的降低妊娠大鼠血浆孕酮浓度和抗早孕作用,给药后24小时内血浆孕酮浓度与对照组相似,全部动物维持妊娠,胚胎大小和数目也与对照组相似。恒速静注15-甲-PGF2α（20微克）于麻醉妊娠大鼠,30分钟后已使子宫卵巢静脉血中孕酮含量由用药前1.271±0.154微克/10分钟下降到0.279±0.083微克/10分钟,给药后60分钟仍维持于低水平。如预先静注 HOG 20国际单位,可使子宫卵巢静脉血中孕酮含量由用药前1.123±0.162微克/10分钟升高到1.496±0.018微克/10分钟,在 HCG作用的基础上再静脉恒速注入15-甲-PGF2α,虽可使子宫卵巢静脉血中孕酮含量下降到1.179±0.042微克/10分钟,但不能降低到

关键词：孕酮血流量孕激素去氢前列腺素女用避孕药妊娠大鼠乙基链烷基甲基

Electrophysiological responses to imidazoline/α2-receptor agonists in rabbit sinoatrial node pacemaker cells

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Acta Pharmacologica Sinica 2003年第12期24卷 43-49页

作者： ZHAO Ding, REN Lei-Ming department of pharmacology, School of Pharmacy, Hebei Medical University, Shijiazhuang 050017, China department of pharmacology School of Pharmacy Hebei Medical University Shijiazhuang 050017

AIM: To compare the effects of moxonidine (Mox), clonidine (Clo), agmatine (Agm), and xylazine (Xyl) on action potentials (AP) of the rabbit sinoatrial node (SAN) pacemaker cells and investigate the contribution of α-adrenoceptors to the cardiac electrophysiologic responses induced by the agonists. METHODS: Intracellular microelectrode technique was used to record AP in the rabbit SAN pacemaker cells. Vasoconstrictive responses to norepinephrine (NE), Mox, Clo, Agm and Xyl were observed in the thoracic aorta and ear vein isolated from rabbits. RESULTS: (1) In the rabbit thoracic aorta, a rank order of potency producing vasoconstrictive responses was NE>Clo>Mox; and a rank order of potency in ear vein was Clo>NE>Xyl=Mox. Agm did not produce any vascular responses in both preparations, and Xyl did not produce vascular responses in the thoracic aorta. (2) Mox, Clo, Xyl, and Agm concentration-dependently decreased the rate of pacemaker firing (RPF), and prolonged APD50and APD90in the rabbit SAN pac

关键词： moxonidine clonidine agmatine xylazine adrenergic alpha-1 receptors adrenergic alpha-2 receptors action potentials sinoatrial node vasoconstriction rabbits

Protective effects of iptakalim,a novel ATP-sensitive potassium channel opener,on global cerebral ischemia-evoked insult in gerbils

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Acta Pharmacologica Sinica 2006年第6期27卷 665-672页

作者： Hua CHEN~(2,4)Yong YANG~(2,4)Hong-hong YAO~2 Xing-chun TANG~2 Jian-hua DING~2 Hai WANG~3 Gang HU~(2,5)2 Laboratory of Neuropharmacology,department of Anatomy,Histology and pharmacology,Nanjing Medical University,Nanjing 210029,China 3 department of Cardiovascular pharmacology,Beijing Institute of pharmacology and Toxicology,Beijing 100850,China department of Anatomy Laboratory of Neuropharmacology Histology and Pharmacology Nanjing Medical University Nanjing China department of Cardiovascular pharmacology Beijing Institute of Pharmacology and Toxicology Beijing China

Aim:To investigate the protective role of iptakalim,a novel ATP sensitive potas-sium channel opener,on global cerebral ischemia-evoked insult in gerbils andglutamate-induced PC 12 cell injury.Methods:Global cerebral ischemia was in-duced by occluding the bilateral common carotid arteries in gerbils for 5 min.Theopen field maze and T-maze were employed to investigate the experimental thera-peutic value of iptakalim on ischemic brain insult（n=8）.The pyramidal cells in thehippocampal CA1 regions were counted to assess the protective effects ofiptakalim.Glutamate released from the gerbil hippocampus and PC12 cells weredetermined by HPLC.Intracellular calcium was measured by Fluo-3 AM with ABio-Rad Radiance 2100TM confocal system in conjunction with a Nikon TE300microscope.Astrocyte glutamate uptake measurements were determined by liq-uid scintillation counting.Results:Iptakalim（0.5-4.0 mg/kg per day,ip）couldreduce the high locomotor activity evoked by ischemia and improve global cere-bral ischemia-induced working memory impairments.Histological studies revealedthat iptakalim could increase the survival neuron in the hippocampus CA1 zone ina dose-dependent manner.Moreover,iptakalim could reverse ischemia-evokedincreases of glutamate in the hippocampus of gerbils.In an in vitro study,iptakalimprotected PC12 cells against glutamate-induced excitotoxicity,reduced the[Ca2+]iincreases,and enhanced the glutamate uptake activity of primary culturedastrocytes.Conclusions:Iptakalim plays a key role in preventing global cerebralischemia-evoked insults in gerbils and glutamate-induced PC12 cell injury by anti-excitotoxicity.Iptakalim might be a promising novel candidate for the preventionand/or treatment of stroke.

关键词： ATP-sensitive potassium channel opener iptakalim global cerebral ischemia neuroprotection excitotoxicity

Construction and Co-expression of Bicistronic Plasmid Encoding Human WEE1 and Stem Cell Factor

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Acta Biochimica et Biophysica Sinica 2005年第2期37卷 107-112页

作者： Ping LEI Wen-Han LI Wen-Jun LIAO Bing YU Hui-Fen ZHU Jing-Fang SHAO Guan-Xin SHEN Laboratory of Molecular and Immuno-pharmacology,department of Immunology and department of pharmacology,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China Laboratory of Molecular and Immuno-pharmacology Department of Immunology and Department of Pharmacology Tongji Medical College Huazhong University of Science and TechnologyWuhan 430030 China

To protect the hematopoietic stem cells(HSCs)from apoptosis induced by chemotherapy andpromote HSC proliferation,bi-functional gene delivery systems are increasingly investigated in gene therapy.In the present study,we constructed a bicistronic vector,pWISG,expressing the anti-apoptotic proteinhuman WEE1(WEE1Hu)and the fusion protein of the proliferation-stimulating stem cell factor(SCF)andenhanced green fluorescent protein(EGFP)separately with internal ribosome entry site(IRES).We firstexamined

关键词： internal ribosome entry site (IRES) human WEE1 (WEE1Hu) stem cell factor (SCF)

Metallothionein mediates cardioprotection of isoliquiritigenin against ischemia-reperfusion through JAK2/STAT3 activation

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Acta Pharmacologica Sinica 2006年第11期27卷 1431-1437页

作者： Wei AN Jing YANG~1 Ying AO department of pharmacology,School of Medicine,Wuhan University,Wuhan 430071,China department of pharmacology School of Medicine Wuhan University Wuhan China

Aim:To examine whether isoliquiritigenin(ISL)can attenuate myocardial ischemia-reperfusion(MI/R)injury in rats by inducing metallothionein(MT)through acti-vation of janus kinase 2(JAK 2)/signal transducers and activators of transcription3(STAT 3)pathway.Methods:The experimental model of MI/R in rats was gener-ated by 30 min of ischemia and reperfusion for 2 h.The mRNA expression of MT,COX-2,and iNOS were measured by RT-PCR.The protein expressions of MT,JAK/STAT,extracellular signal-regulated kinase(ERK),and Akt were determinedby Western blotting in the absence or presence of a JAK kinase inhibitor,tyrphostinAG490(1.0 mg/kg,iv,1h before ischemia).Results:Pretreatment with ISL mark-edly decreased the severity of reperfusion-induced arrhythmias and myocardialinfarct size.In the ISL 20 mg/kg group,the activities of lactate dehydrogenase(LDH)and creatinine phosphokinase(CPK)were reduced by 38.4% and 51.3%when compared with the vehicle group.Increased JAK 2/STAT 3 phosphoryla-tion was accompanied by increased synthesis of MT but not of COX-2 or iNOS inISL-treated groups.AG490 can significantly weaken ISL-induced cardioprotectionand prevent the increase of MT expression and JAK 2/STAT 3 phosphorylation.Conclusion:ISL protected MI/R injury through activation of JAK 2/STAT 3 sig-nal transduction pathway,which might be involved in mediating the upregulationof MT expression.

关键词： isoliquiritigenin myocardial ischemiareperfusion metallothionein janus kinase STAT3 transcription factors

Influence of Trace Amount of Calponin on Smooth Muscle Myosin in Different States

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Acta Biochimica et Biophysica Sinica 2004年第8期36卷 529-536页

作者： Jing-Xian YANG, Xiao-Hua FENG, Ying ZHANG, and Yuan LIN department of pharmacology, Dalian Medical University, Dalian 116027, China department of pharmacology Dalian Medical UniversityDalian 116027 China

Calponin (CaP), a thin filament-associated protein, is thought to be involved in modulating smooth muscle contractile activity, but the role and mechanism keep unknown. In this study, trace amount of calponin (TAC) was found to obviously influence myosin in different states in Ca2+-independent manner, suggesting a high efficient interaction between TAC and myosin. In this assay, the lowest ratio of CaP vs. myosin was 1:10,000, with the concentration of CaP 10,000-fold lower than that used previously. Myosin phosphorylation, myosin Mg2+-ATPase activity and protein binding activity were detected to determine the effects of TAC on the myosin in different states. The amount of precipitated myosin that bound to TAC was used as the index to determine the interaction between myosin and TAC in binding assay. Our data showed that in the absence of actin, TAC significantly increased the precipitation of unphosphorylated myosin, Ca2+- dependently or independently phosphorylated myosin by MLCK, and stimulated the Mg2+-ATPase activities of these myosins slightly but significantly. However, no obvious change of precipitation of myosin phospho- rylated by PKA was observed, indicating the relatively selective effect of TAC. In the presence of actin, the increase of myosin precipitations was abolished, and no obvious change of actin precipitations and actin- activated myosin Mg2+-ATPase activities were observed implicating the high efficiency of TAC on myosin being present in the absence of actin. Although we can not give conclusive comments to our results, we propose that the high efficiency of TAC-myosin interaction is present when actin is dissociated from myosin, even if CaP/myosin ratio is very low; this high efficient interaction can be abolished by actin. However, why and how TAC can possess such a high efficiency to influence myosin and how the physiological significance of the high efficiency of TAC is in regulating the interaction between myosin and actin remain to be investigated.

关键词： trace amount of calponin protein binding phosphorylation myosin Mg2+-ATPase

Arecoline inhibits catecholamine release from perfused rat adrenal gland

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Acta Pharmacologica Sinica 2006年第1期27卷 71-79页

作者： Dong-yoon LIM II-sik KIM department of pharmacology,College of Medicine,Chosun University,Gwangju 501-759,Korea department of pharmacology College of Medicine Chosun University Gwangju Korea

Aim:To study the effect of arecoline,an alkaloid isolated from Areca catechu,onthe secretion of catecholamines (CA) evoked by cholinergic agonists and themembrane depolarizer from isolated perfused rat adrenal gland.Methods:Adrenalglands were isolated from male Sprague-Dawley rats.The adrenal glands wereperfused with Krebs bicarbonate solution by means of a peristaltic pump.The CAcontent of the perfusate was measured directly using the fluorometric method.Results:Arecoline (0.1-1.0 mmol/L) perfused into an adrenal vein for 60 min pro-duced dose-and time-dependent inhibition in CA secretory responses evoked byacetylcholine (ACh) (5.32 mmol/L),1.1-dimethyl-4-phenyl piperazinium iodide(DMPP) (100μmol/L for 2 min) and 3-(m-choloro-phenyl-carbamoyl-oxy)-2-butynyltrimethyl ammonium chloride (McN-A-343)(100μmol/L for 2 min).However,lowerdoses of arecoline did not affect CA secretion of high K~+(56 mmol/L);higherdoses greatly reduced CA secretion of high K~+.Arecoline also failed to affectbasal catecholamine output.Furthermore,in adrenal glands loaded with arecoline(0.3 mmol/L),CA secretory response evoked by Bay-K-8644 (10μmol/L),an activa-tor of L-type Ca2+channels,was markedly inhibited,whereas CA secretion bycyclopiazonic acid(10μmol/L),an inhibitor of cytoplasmic Ca2+-ATPase,was notaffected.Nicotine (30μmol/L),which was perfused into the adrenal gland for 60min,however,initially enhanced ACh-evoked CA secretory responses.As timeelapsed,these responses became more inhibited,whereas the initially enhancedhigh K~+-evoked CA release diminished.CA secretion evoked by DMPP and McN-A-343 was significantly depressed in the presence of nicotine.Conclusion:Arecoline dose-dependently inhibits CA secretion from isolated perfused rat ad-renal gland evoked by activation of cholinergic receptors.At lower doses arecolinedoes not inhibit CA secretion through membrane depolarization,but at largerdoses it does.This inhibitory effect of arecoline may be mediated by blocking thecalcium influx into the rat adrenal medullary chromaffin ce

关键词： arecoline catecholamine secretion adrenal gland nicotine