刘俊田
心脑血管药理学
个性化签名
- 姓名:刘俊田
- 目前身份:
- 担任导师情况:
- 学位:
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学术头衔:
博士生导师
- 职称:-
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学科领域:
药物化学
- 研究兴趣:心脑血管药理学
刘俊田,教授,博士研究生导师,享受国务院特殊津贴专家。曾任西安交通大学医学院基础医学部主任,现任西安交通大学医学院药理系生化药理研究室主任,中国药理学会副理事长,陕西省药理学会理事长,陕西省自然科学学会研究会副理事长,陕西省毒理学会副理事长,陕西省科协委员。国家科技奖评审专家,中华医学科技奖、中华医学青年奖评审专家。国家科技部项目、科技部国际科技合作计划、国家留学基金委、卫生部重大科技专项、西安市科技计划项目、西安高新区项目评审专家,教育部学位中心“学位与研究生教育”评估专家,“中国中文核心期刊”评审专家,国家自然科学基金评审专家,《中国药理学通报》、《中国实验方剂学杂志》等审稿人。
从事药理学教学与研究,研究方向为心脑血管药理学。公开发表文章164篇,其中SCI收录29篇;参编和主编教材及专著36部,培养硕士、博士研究生37名。
主持和参与国家自然科学基金、教育部博士点专项科研基金、卫生部科学研究基金、陕西省自然科学基金等科研项目25项,参与新药研发近百项。曾获得陕西省科技进步三等奖一项,陕西高等学校科技进步奖四项,西安交通大学自然科学二等奖一项,陕西省自然科学三等优秀学术论文奖一项,陕西省高等教育学会优秀高教科研成果三等奖。
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成果数
6
【期刊论文】3,6-(二甲氨基)二苯并碘杂六环葡萄糖酸盐抗心律失常作用
刘俊田, 苟伟*, 李西宽, 杜克辛, 邓秀玲, 侯自杰
中国药理学与毒理学杂志,2001,6(3):176-179,-0001,():
-1年11月30日
在氯化钡(BaCl2),氯仿-肾上腺素,毒毛花苷G,乌头碱,乙酰胆碱-氯化钙(ACh-CaCl2)5种实验性心律失常模型上观察了3,6-(二甲氨基)二苯并碘杂六环葡萄糖酸盐(IHC-93)对抗心律失常的作用。结果表明IHC-930.25和0.50mg·kg-1均可对抗ACh-CaCl2诱发的小鼠房颤(扑);明显缩短BaCl2诱发的大鼠室性心律失常持续时间;对氯仿肾上腺素诱发家兔的心律失常有预防及缓解作用;能提高毒毛花苷G致豚鼠室性早搏,室性心动过速,室颤和心搏停止的用量;能提高乌头碱导致室性早搏用量,对室性心律失常有部分对抗作用。
3,, 6-(, 二甲氨基), -二苯并碘杂六环葡萄糖酸盐, 抗心律失常药
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刘俊田, *‡W. Paul, †‡P. Gresele, †‡S. Momi, **G. Bianchi & l*‡C.P. Page
Br. J. Pharmacol. (I993), 110, 1565-1571,-0001,():
-1年11月30日
1 Administration of bovine thrombin (100ukg-1) into the carotid artery of rabbits induces a sustained accumulation of Indium-labelled platelets within the cranial vasculature over the subsequent 3h. 2 Intracarotid (i.c.) administration of defibrotide (64mg kg-1 bolus plus 64mg kg-1h-1 for 1h) prior to i.c. thrombin (100ukg-1) significantly reduces the ability of thrombin to induce cranial thromboembolism in rabbits. 3 Intravenous (i.v.) administration of thrombin (20ukg-1) in rabbits induces a reversible accumulation of radiolabelled platelets into the thoracic circulation which is significantly reduced by i.v. administration of defibrotide (64mg kg-1 bolus plus 64mg kg-1h-1 for 1h) prior to i.v. thrombin. In contrast, platelet accumulation in response to adenosine diphosphate (ADP; 20pg kg-1, i.v.) or platelet activating factor (PAF; 50ng kg1, i.v.) is not significantly affected by this treatment. 4 Intravenous administration of the nitric oxide (NO)-synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 10mgkg-1) potentiates platelet accumulation induced by low dose thrombin (10ukg-1, i.v.) within the pulmonary vasculature of rabbits. The potentiated response is significantly abrogated following pretreatment with defibrotide (64mg kg-1 bolus plus 64 mg kg-1 h-for 1h, i.v.). 5 Intravenous injection of human thrombin (1250u kg-1) to mice induces death within the majority of animals which is significantly reduced by pretreatment with defibrotide (150-175mg kg1, i.v.). In contrast, death induced by i.v. collagen (1.25mg kg-1) plus adrenaline (75gg kg-1) is not significantly affected by defibrotide pretreatment. 6 The inhibitory effect of defibrotide in mice is abolished following concomitant treatment with the inhibitor of fribrinolysis, tranexamic acid (100mg kg-1, i.v.), but is unaffected following treatment with the cyclo-oxygenase inhibitor, aspirin (300mg kg-1, i.p.). 7 The protective effect of defibrotide against thrombin-induced thromboembolism in the mouse is potentiated by recombinant tissue-plasminogen activator (rt-PA; 1 mg kg-1, i.v.) or unfractionated heparin (10ukg-1, i.v.) administration. 8 The results suggest that defibrotide may possess antithrombotic activity on thrombin-induced thromboembolism which, at least in the mouse, may be partially mediated via induction of the fibrinolytic pathway.
[1]-Indium, platelets, defibrotide, thrombosis, fibrinolysis
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【期刊论文】川芎嗪对缺氧缺糖状态下培养的血管内皮细胞ECV2304的影响
刘俊田, 林蓉, 甘伟杰, 王维蓉
中国中药杂志,2004,5(5):462-465,-0001,():
-1年11月30日
目的:观察缺氧缺糖条件下血管内皮细胞(ECV2304)释放乳酸脱氢酶(LDH)、一氧化氮(NO)、丙二醛(MDA)水平和细胞膜流动性的变化及川芎嗪对它们的影响。方法:缺氧缺糖诱导血管内皮细胞损伤,自动生化分析仪测定培养液和细胞层中LDH活性;用比色法测定细胞培养液中NO水平;用荧光法检测细胞内脂质过氧化产物MDA以评价脂质过氧化程度;荧光偏振法测定内皮细胞膜流动性。结果:缺氧缺糖引起的血管内皮细胞LDH释放增加、MDA生成增多和膜流动性增高,NO水平降低。而川芎嗪可抑制缺氧缺糖引起的血管内皮细胞释放LDH,MDA生成和降低细胞膜流动性,提高NO水平。结论:川芎嗪可保护缺氧缺糖诱导血管内皮细胞的损伤,其作用机制有待进一步研究。
川芎嗪, 血管内皮细胞ECV2304, 膜流动性, 缺氧缺糖
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刘俊田, Rong LIN, *, a Juntian LIU, a Weijie GAN, a and Guangde YANG b
Biol. Pharm. Bull. 27(10) 1537-1543 (2004),-0001,():
-1年11月30日
Inflammation plays a pivotal role in the formation of atherosclerosis. In addition to being a risk marker for cardiovascular diseases, the role of C-reactive protein (CRP) in atherogenesis has been supported by more recent data. CD40-CD40L system is proven to be an important mediator of several auto-immune and chronic inflammation diseases. Interruption of CD40–CD40L signaling pathway not only reduces the initiation and progression of atherosclerotic lesions, but also modulates plaque architecture. By using a flow cytometry and western blotting, we found that incubation of human umbilical vein endothelial cells (HUVECs) with CRP resulted in a timeand dose-dependent increase in the cell-surface expression of CD40 and CD40L. In addition, CRP (25mg/ml) increased gelatinolytic activities of MMP-2 and MMP-9. Anti-CD40 antibody significantly reversed the upregulated activities of MMP-2 and MMP-9 induced by CRP with gelatin zymography. Furthermore, lovastatin (10-7, 10-6, 10-5mol/l) and fenofibrate (5×10-5, 10-4, 2×10-4mol/l) significantly diminished the expression of CD40, CD40L and gelatinase activities (MMP-2, MMP-9) induced by CRP in HUVECs. In conclusion, our data provide evidence to support the direct pro-inflammatory effects of CRP via CD40-CD40L signaling pathway involved in the pathogenesis of atherosclerosis, and lovastatin and fenofibrate possess anti-inflammatory effects independent of their lipid-lowering action.
C-reactive protein (, CRP), , CD40, CD40L, MMP-9, lovastatin, fenofibrate
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【期刊论文】红毛七提取物对H202损伤内皮细胞核转录因子-KB的表达和NO生成的影响
刘俊田, 林蓉, 贺浪冲, 甘伟杰, 杨广德
中国药学杂志,2004,11(11):826-828,-0001,():
-1年11月30日
目的 观察红毛七的提取物(HMO4)对H202损伤内皮细胞核转录因子-KB的表达和一氧化氮(NO)、一氧化氮合酶(NOs)的影响。方法 用H2O2造成血管内皮细胞损伤模型,采用MTT法观察HMO-4对血管内皮细胞活性的影响;用比色法测定细胞培养液中NO,NOs含量;免疫细胞化学法观察内皮细胞核转录因子-kB的表达。结果 H2O2对血管内皮细胞具有损伤作用,HMO4在一定剂量内减少细胞的死亡;HMO-4还可促进H2O2损伤的血管内皮细胞内No,Nos释放的增加和抑制核转录因子-kB的表达的加强。结论 HMO-4对H2O2损伤的血管内皮细胞具有保护作用,其机制可能与其增加NO,N0s释放和转录因子-KB的表达有关。
红毛七, 内皮细胞, 核转录因子-KB
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刘俊田, Rong LIN, *, a, b Juntian LIU, a Ning PENG, a Guangde YANG, c Weijie GAN, a and Weirong WANGa
Biol. Pharm. Bull. 28(9) 1630-1634 (2005),-0001,():
-1年11月30日
The role of C-reactive protein (CRP) in atherogenesis has been supported by more recent data. Some studies have demonstrated marked up-regulation inflammatory responses in endothelial cells subjected to CRP. The nuclear factor-k B (NF-k B) signal transduction is known to play a key role in the expression of these proatherogenic entities. Statins have anti-inflammatory properties independent of their cholesterol-lowering effects. Therefore, we studied the effects of CRP and lovastatin on NF-k B activation in human umbilical vein endothelial cells (HUVECs). By using an electrophoretic mobility shift assays (EMSA), we found that CRP (50mg/ml) increased activation of NF-k B and degradation of inhibitory kappa B (Ik B) in HUVECs, reaching a maximal effect after the incubation with CRP for 1 h. Lovastatin (10.5mol/l) diminished NF-k B activation induced by CRP. Furthermore, lovastatin may block NF-k B activation by causing a stabilization of the Ik B-a in cellular cytoplasm with western blotting analysis. Preincubation of HUVECs with pyrrolidinethiocarbamate (PDTC, NF-k B inhibitor) diminished CD40 expression induced by CRP with flow cytometry. Our results suggest that CRP increases activation of NF-k B and induces CD40 expression in HUVECs partly via activation of NF-k B. Lovastatin, through the inhibition of NF-k B activation, reduces the inflammation involved in the pathogenesis of atherosclerosis.
lovastatin, C-reactive protein (, CRP), , nuclear factor-k B (, NF-k B), , CD40
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