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SD大鼠每天ip THB 30 mg·kg~(-1)共3 d或5 d后,使ADP诱导的血小板聚集程度降低;同剂量ip 1 d,3 d或5 d后,使AA诱导的血小板聚集程度降低,THB在体外抑制AA,ADP和胶原诱导的兔血小板聚集,IC_(50)分别为0.86,1.31和1.10 mmol·L~(-1) THB能抑制AA诱导的兔血小板生成血栓素B_2 THB 15—30 mg·kg~(-1)iv明显抑制大鼠静脉血栓的形成。 相似文献
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N-(4-胍基丁基)丁香酰胺对家兔血小板聚集性的影响 总被引:1,自引:0,他引:1
目的考察N-(4胍基丁基)丁香酰胺对家兔体外血小板聚集的影响。方法以盐酸益母草碱为阳性对照,以二磷酸腺苷(Adenosine Diphosphate,ADP),花生四烯酸(Arachidonic Acid,AA),胶原(Collagen,COL)为诱导剂诱导家兔体外血小板聚集,采用Born氏比浊法,利用血小板聚集仪测定5 min血小板最大聚集率,观察不同浓度的N-(4胍基丁基)丁香酰胺对家兔体外血小板聚集的影响。结果不同浓度N-(4胍基丁基)丁香酰胺对ADP、AA、COL诱导的家兔体外血小板聚集均有一定抑制作用。结论 N-(4胍基丁基)丁香酰胺具有一定的体外抗血小板聚集的作用。 相似文献
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目的:研究阿司匹林铜(CuAsp)对血小板聚集性的影响及其机制.方法:用Born氏法测定CuAsp对兔血小板聚集性的影响.用荧光光度法和放射免疫法观察CuAsp对兔血小板5羟色胺的释放和TXB2的产生及血浆中TXB2和6ketoPGF1α水平的影响.结果:CuAsp体外呈浓度依赖性抑制花生四烯酸(AA)诱导的血小板聚集和5羟色胺的释放(IC50分别为17和19μmol·L-1,95%可信限为9-33和10-30μmol·L-1),且抑制TXB2的产生(P<005).CuAsp10mg·kg-1灌胃选择性抑制AA诱导聚集.降低血浆TXB2,同时升高6ketoPGF1α的水平(P<005).结论:CuAsp体内外均有比Asp更强的抗血小板聚集作用. 相似文献
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异钩藤碱对血小板聚集与血栓形成的抑制作用 总被引:2,自引:2,他引:2
目的研究异钩藤碱(isorhynchophylline,Isorhy)对血小板聚集与血栓形成的影响,并探讨其机制。方法以比浊法测定Isorhy体外给药对大鼠血小板聚集的影响;采用动-静脉旁路血栓形成法制作大鼠血栓模型,观察Isorhy对血栓形成的作用;以放免法测定Isorhy对ADP作用下cAMP含量的影响。结果Isorhy0.65mmol.L-1和1.30mmol.L-1对ADP(1.5×10-5mol.L-1)和凝血酶(thrombin,Thr,3U.ml-1)诱导的大鼠血小板聚集均有抑制作用(P<0.01)。静脉注射Isorhy10mg.kg-1和5mg.kg-1可明显降低大鼠血栓形成湿重(P<0.01)。Isorhy0.33~1.30mmol.L-1可升高ADP作用后的血小板cAMP浓度(P<0.01)。结论Isorhy明显抑制血小板聚集与大鼠血栓形成,其抗ADP所致血小板聚集的作用机制至少部分地与升高cAMP水平有关。 相似文献
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目的:研究尼莫地平(Nim)对大鼠体内血小板聚集和动脉血栓形成的影响.方法:比浊法测定血小板的聚集率和抑制率;电刺激法测定Nim对体内动脉血栓形成的影响,放免法测定Nim对血浆6酮前列腺素F1α和血栓素B2(6ketoPGF1α/TXB2)含量的影响.结果:Nim45,9,18和36mg·kg-1·d-1ig4d可显著抑制血小板的聚集.IC50(95%可信限)为26(9-44)mg·kg-1.Nim45,9,18mg·kg-1·d-1ig4d可显著延长电刺激诱导的颈动脉血栓形成时间.Nim9和18mg·kg-1可明显改善血浆中6ketoPGF1α/TXB2的比值.结论:Nim抗血栓作用部分与改善6ketoPGF1α/TXB2比值有关. 相似文献
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目的:研究阿司匹林铜(CuAsp)对血小板聚集性的影响及其机制,方法;用Born氏法测定CuAsp对兔血小板聚集性的影响,用荧光光度法和放射免疫法观察CuAsp对兔血小板5-羟色胺的释放和TXB2的产生及血浆中TXB2和6-keto-PGF1α水平的影响,结果:CuAsp体外呈浓度依赖性抑制花生四烯酸(AA)诱导的血小板聚集和5-羟色胺的释放(IC50分别为17和19μmol.L^-1,95%可信 相似文献
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O Irino K Saitoh T Hayashi K Ohkubo 《Nihon yakurigaku zasshi. Folia pharmacologica Japonica》1985,85(5):379-385
The effects of dl-erythro-4-benzyl-alpha-(4-hydroxyphenyl)-beta-methyl-l-piperidine-eth anol tartrate (ifenprodil tartrate) on rabbit platelet aggregation in vitro and ex vivo were studied. Ifenprodil tartrate inhibited platelet aggregation in vitro induced by ADP, collagen and epinephrine. It also inhibited 5-hydroxytryptamine (5-HT) uptake into platelets and 5-HT release from platelets. Since these inhibitory effects of ifenprodil tartrate on the functions of rabbit platelets were similar to the effects of imipramine, the effects of ifenprodil tartrate may be due to the stabilizing action of ifenprodil tartrate on the platelet membrane. The platelet aggregation by ADP was significantly inhibited in rabbits after oral administration of ifenprodil tartrate, the maximal plasma level of ifenprodil being reached at 20 ng/ml ex vivo, while the maximal level was only 1/40 of the minimal concentration of ifenprodil tartrate necessary to inhibit platelet aggregation in vitro. These results indicate that factors other than ifenprodil tartrate acting directly on the platelets (e.g., PGI2 which is an endogenous inhibitor of platelet aggregation) are involved in inducing the inhibitory effects of ifenprodil tartrate on platelet aggregation ex vivo. The effects of ifenprodil tartrate on both PGI2 release from the aorta and the inhibitory effects of PGI2 on platelet aggregation in vitro were investigated: PGI2 was found to intensify the inhibitory effects of ifenprodil tartrate on platelet aggregation in vitro, but there was little effect, if any, on PGI2 release. Therefore, it is considered that the ex vivo effects of ifenprodil tartrate might be due to its interaction with endogenous PGI2 in the blood. 相似文献
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目的:研究尼莫地平(Nim)对大鼠体内血小板聚集和动脉血栓形成的影响。方法:比浊法测定血小板的聚集率的抑制率;电刺激法测定Nim对体内动脉血栓形成的影响,放免法测定Nim对血浆6-酮前列腺素F1α和血栓素B2(6-keto-PGF1α/TXB2)mg·kg^-1·d^-1 ig4d可显著抑制血小板的聚集。IC50(95%)可信限)为26(9-44)mg·kg^-1.Nim4.5,9,18mg·kg 相似文献
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目的 研究丹七片对家兔和大鼠血小板聚集的影响,并探讨其作用机制.方法 以阿魏酸钠为阳性对照,采用比浊法测定丹七片对凝血酶和胶原诱导的血小板聚集的影响,采用酶联免疫法测定丹七片对凝血酶作用下的血小板内环磷酸腺苷(cAMP)含量的影响.结果 丹七片可明显抑制由凝血酶和胶原诱导的血小板聚集;丹七片可升高凝血霉作用下的血小板内cAMP含量.结论 丹七片抑制由凝血酶和胶原诱导的血小板聚集的作用机制与升高血小板内cAMP的含量有关. 相似文献
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Lee WM Kim SD Park MH Cho JY Park HJ Seo GS Rhee MH 《The Journal of pharmacy and pharmacology》2008,60(11):1531-1536
Ginsenoside Rg3, a single ginseng saponin, is known to be a major anti-platelet component of protopanaxadiol that is isolated from Korean red ginseng. In this study, we investigated whether dihydroginsenoside Rg3, a stable chemical derivative of ginsenoside Rg3, also demonstrated anti-platelet activity. Dihydroginsenoside Rg3 inhibited thrombin-induced platelet aggregation in a concentration-dependent manner with an IC50 (concentration producing 50% inhibition) of 18.8 +/- 0.4 microM. Ginsenoside Rg3 inhibited platelet aggregation which was induced by thrombin (0.1 U mL(-1)) with an IC50 of 40.2 +/- 0.9 microM. We next determined whether dihydroginsenoside Rg3 affected different types of ligand-induced platelet aggregation. We found that dihydroginsenoside Rg3 inhibited collagen-induced platelet aggregation with an IC50 of 20.0 +/- 0.9 microM. To elucidate the inhibitory mechanism of dihydroginsenoside Rg3 on aggregation, we analysed its downstream signalling pathway. It was interesting to note that dihydroginsenoside Rg3 elevated cyclic AMP production in resting platelets, but did not affect cyclic GMP production. In addition, we found that dihydroginsenoside Rg3 potently suppressed phosphorylation of extracellular signal-regulated kinase 2 (ERK2), which was stimulated by collagen (2.5 microg mL(-1)), but not of p38 mitogen-activated protein kinase. Taken together, our results indicate that dihydroginsenoside Rg3 potently inhibited platelet aggregation via the modulation of downstream signalling components such as cAMP and ERK2. 相似文献
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Inhibitory mechanisms of activated matrix metalloproteinase-9 on platelet activation 总被引:1,自引:0,他引:1
The intracellular mechanisms underlying the signaling pathways of activated matrix metalloproteinase-9 (MMP-9) in platelets are not yet completely understood. Therefore, the aim of this study was to further examine the effects of activated MMP-9 in preventing platelet aggregation. In this study, activated MMP-9 time-dependently (3-60 min) inhibited platelet aggregation in washed human platelet suspensions stimulated by agonists. However, activated MMP-9 had no significant effect on the binding of FITC-triflavin to the platelet glycoprotein IIb/IIIa complex. Triflavin is a specific antagonist of the glycoprotein IIb/IIIa complex purified from snake venom. Moreover, activated MMP-9 (21 and 90 ng/ml) markedly decreased the fluorescence intensity of platelet membranes tagged with diphenylhexatriene. The thrombin-evoked increase in pHi was inhibited in the presence of activated MMP-9 (21 and 90 ng/ml). In addition, activated MMP-9 (21 and 90 ng/ml) markedly reduced the electron spin resonance (ESR) signal intensity of hydroxyl radicals in collagen (1 mug/ml)-activated platelets. These results indicate that the antiplatelet activity of activated MMP-9 may involve the following pathways: (1) activated MMP-9 may initially induce conformational changes in platelet membranes and hydroxyl radical formation, leading to inhibition of platelet aggregation; and (2) activated MMP-9 also inhibits the Na(+)/H(+) exchanger, leading to reduced intracellular Ca(2+) mobilization, and ultimately to inhibition of platelet aggregation. This study further provides new insights concerning the effects of activated MMP-9 on platelet aggregation. 相似文献
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目的研究中华眼镜蛇毒金属蛋白酶atrase A对血小板聚集的影响及其相关的机制。方法测定atrase A对二磷酸腺苷、胶原、血小板活化因子、花生四烯酸、瑞斯托霉素、凝血酶诱导血小板聚集的影响情况,并通过蛋白质免疫印迹检测atrase A对血小板膜糖蛋白和血管假血友病因子的酶切情况。结果中华眼镜蛇毒金属蛋白酶atrase A能明显抑制由瑞斯托霉素和凝血酶诱导的血小板聚集,这种抑制作用呈量效、时效关系。而atrase A和血小板预孵5min后对二磷酸腺苷、胶原、血小板活化因子、花生四烯酸诱导的血小板聚集有微弱的抑制作用,预孵时间延长至30min对血小板聚集有明显的抑制作用。蛋白质免疫印迹结果显示atrase A能特异性酶切血小板膜糖蛋白GPIb,但对vWF几乎没有酶切作用。结论中华眼镜蛇毒金属蛋白酶atrase A对二磷酸腺苷、胶原、血小板活化因子、花生四烯酸、瑞斯托霉素、凝血酶诱导的血小板聚集均有抑制作用,其中对瑞斯托霉素和凝血酶诱导的血小板聚集具有明显的抑制作用,其机制是通过酶切血小板膜糖蛋白GPIb。 相似文献
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The activation of human platelets by 5-hydroxytryptamine (5-HT) is not accompanied by detectable release of ATP or TXB2. The process is unaffected by cyclooxygenase, thromboxane synthetase or combined cyclooxygenase/lipoxygenase inhibition (suprofen, indomethacin, R 19091, dazoxiben, N.D.G.A, BW755C, esculetin), indicating the absence of involvement of arachidonic acid metabolites. Transmembrane Ca2+-entry blockers (flunarizine, nifedipine, nimodipine) have no effect either, indicating that the activator calcium released by 5-HT comes from intracellular stores. The 5-HT-induced platelet activation is inhibited by stimulators of adenylate cyclase (PGE1, PGE2, isoprenaline, adenosine) and inhibitors of cAMP phosphodiesterase (papaverine, anagrelide, RA233), indicating that also for this type of platelet activation cAMP behaves as a unidirectional, inhibitory regulator. 相似文献