李元建
科研方向为心血管药理,主要研究内容为心血管新药研发及药物作用机制。
个性化签名
- 姓名:李元建
- 目前身份:
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学术头衔:
博士生导师
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学科领域:
药物化学
- 研究兴趣:科研方向为心血管药理,主要研究内容为心血管新药研发及药物作用机制。
李元建,男,1953年1月生,1973年毕业于湖南医学院,1985年获医学硕士学位,1989年获美国心脏学会博士后资助,在加州大学欧文分校博士后学习工作两年(1989-1991年),1994年晋升为教授。现任中南大学药学院院长,药理学教授,博士生导师,国家新药评审专家,国家重点新产品评审专家,享受政府特殊津贴,卫生部有突出贡献的中青年专家,湖南省优秀教师(1998年)。兼任湖南省心血管研究重点实验室主任,中国药理学会心血管专业委员会副主任委员,湖南省药学会副理事长,湖南省生理科学学会副理事长。《国外医学—生理、病理科学与临床分册》主编,《中国药理学与毒理学杂志》、《中国动脉硬化杂志》、《中南大学学报—医学版》、《中国药理通讯》等杂志编委。主编与参编教材或专著11部。先后获卫生部青年科研基金、美国心脏学会博士后资助、教育部优秀年轻教师基金及重点跟踪资助、教育部跨世纪优秀人才培养计划基金、教育部重大项目、国家自然科学基金面上与重点项目、湖南省自然科学基金、湖南省重点实验室基金等10余项基金。科研方向为心血管药理,主要研究内容为心血管新药研发及药物作用机制。国内外首次报道动脉粥样硬化动物血中内源性一氧化氮合酶抑制物非对称性二甲基精氨酸浓度升高,提出内源性非对称性二甲基精氨酸可能是动脉粥样硬化形成的促进物以及寻找新药的靶点;较系统的研究了降钙素基因相关肽的心血管作用,提出降钙素基因相关肽为一种内源性心肌保护物质,参与缺血预适应心肌保护的调节,介导硝酸甘油的心血管效应,并发现中药吴茱萸中的重要药理活性成分吴茱萸次碱抗高血压作用是通过激动辣椒素受体促进降钙素基因相关肽合成与释放。先后获省部级科研成果13项,包括教育部自然科学奖二等奖3项,三等奖1项;卫生部科技奖二等奖3项,三等奖1项;湖南省科技进步奖二等奖4项,三等奖1项。指导的研究生获全国或省级优秀论文20余人次,其中1人获全国优秀博士论文奖,3人获全国优秀博士论文提名奖, 获湖南省教学成果奖2项。发表科研论文150余篇,其中被SCI收录论文120余篇。
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成果阅读
181
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成果数
5
【期刊论文】CGRP-mediated cardiovascular effect of nitroglycerin
李元建, Yuan-Jian Li, Yan-Hua Du
Medical Hypotheses (2003) 60 (5), 693-698,-0001,():
-1年11月30日
Summary Organic nitrates, including nitroglycerin, produce vascular relaxation by releasing nitric oxide in vascular tissues near the plasma member of smooth muscle cells of veins and arteries. Calcitonin gene-related peptide (CGRP), a major transmitter in capsaicin-sensitive sensory nerves, is widely distributed in cardiovascular tissues and the release of CGRP is regulated by multiple autacoids including nitric oxide (NO). CGRP exerts complex cardiovascular effects including potent vasorelaxation and protective effects on myocytes and endothelial cells. Nitroglycerin activates sensory nerves fibres to release CGRP by generating NO and increasing cGMP
level,, and that the cardiovascular effects of nitroglycerin are partly mediated by endogenous CGRP.,
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李元建, Zhong Dai, Hui-Qing Zhu, De-Jian Jiang, Jun-Ling Jiang, Han-Wu Deng, Yuan-Jian Li*
International Journal of Cardiology 96(2004)223-227,-0001,():
-1年11月30日
Previous studies have shown that endothelial dysfunction is associated to an increase of endogenous nitric oxide synthase (NOS) inhibitor level and estrogen reduces impairment of the endothelium due to oxidized low-density lipoprotein (LDL). The purpose of the present study was to investigate the effect of estradiol on endothelial dysfunction and the increased level of asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, induced by LDL. Male Sprague-Dawley rats were treated with a single injection of native LDL (4mg/kg) for 48 h. Vasodilator responses to acetylcholine in the aortic rings and serum levels of ADMA and malondialdehyde (MDA) were determined. Treatment with native LDL markedly reduced endothelium-dependent relaxation to acetylcholine in the isolated rat thoracic aortic rings and increased serum levels of ADMA and MDA (P<0.01). Pretreatment with 17h-estradiol (0.1 or 0.3mg/kg) significantly attenuated inhibition of vasodilator responses to acetylcholine and elevation of both ADMA and MDA concentration by LDL (P<0.01). These results suggest that estradiol possesses a protective effect on the endothelium and the protective effect is related to reduction of ADMA concentration by inhibition of lipid peroxidation.
17h-Estradiol, Asymmetric dimethylarginine, Low-density lipoprotein, Endothelium
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李元建, Jun Peng, Rong Lu, Han-Wu Deng, Yuan-Jian Li *
European Journal of Pharmacology 436(2002)89-96,-0001,():
-1年11月30日
Recent study has shown that monophosphoryl lipid A-induced delayed preconditioning enhanced preservation with cardioplegia and that the protective effects of monophosphoryl lipid A were related to stimulation of calcitonin gene-related peptide (CGRP) release. The purpose of the present study was to explore whether the elevated release of CGRP induced by monophosphoryl lipid A is secondary to stimulation of CGRP synthesis via the nitric oxide (NO) pathway and to characterize the isoform of CGRP. Sprague-Dawley rats were pretreated with monophosphoryl lipid A 24h before the experiment, and then the left main coronary artery of rat hearts was subjected to 1 h occlusion followed by 3 h reperfusion. Infarct size, plasma creatine kinase activity, the plasma level of CGRP, and the expression of CGRP isoforms (aand b-CGRP) mRNA in lumbar dorsal root ganglia were measured. Pretreatment with monophosphoryl lipid A (500mg/kg, i.p.) significantly reduced infarct size and creatine kinase release. Monophosphoryl lipid A caused a significant increase in the expression of a-CGRP mRNA, but not of b-CGRP mRNA, concomitantly with an increase in plasma concentrations of CGRP, and the increased level of CGRP expression happened before stimulation of CGRP release. The effect of monophosphoryl lipid A was completely abolished by pretreatment with Lnitroarginine methyl ester (L-NAME, 10 mg/kg, i.p.), an inhibitor of NO synthase or capsaicin (50 mg/kg, s.c.), which selectively depletes transmitters in capsaicin-sensitive sensory nerves. The results suggest that the delayed cardioprotection afforded by monophosphoryl lipid A involves the synthesis and release of CGRP via the NO pathway, and that the protection is mainly mediated by the a-CGRP isoform.
CGRP (, calcitonin gene-related peptide), , Monophosphoryl lipid A, Preconditioning, Ischemia– reperfusion, Capsaicin, Nitric oxide (, NO),
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李元建, Zhi-Hong Zhou, Jun-lin Jiang, Jun Peng, Han-Wu Deng, Yuan-Jian Li*
European Journal of Pharmacology 439(2002)129-134,-0001,():
-1年11月30日
Previous studies have shown that the development of tolerance to nitroglycerin is related to a decrease in the release of endogenous calcitonin gene-related peptide (CGRP). In the present study, we explored whether endogenous CGRP is involved in reversal of tolerance to nitroglycerin with N-acetylcysteine or captopril in rats in vivo and vitro. Tolerance was induced by exposure to nitroglycerin (4.4
Tolerance, Nitroglycerin, CGRP (, calcitonin gene-related peptide), , N-acetylcysteine, Captopril
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李元建, Jun Peng, Jun Xiao, Feng Ye, Han-Wu Deng, Yuan-Jian Li)
European Journal of Pharmacology 407 2000. 303-308,-0001,():
-1年11月30日
Previous investigations have demonstrated that calcitonin gene-related peptideCGRP.plays an important role in the mediation of ischemic preconditioning in rats. In the present study, we examined signal transduction pathways of CGRP-mediated ischemic preconditioning. Thirty minutes of global ischemia and 40 min of reperfusion caused a dramatic decrease in myocardial function, and a significant increase in the release of cardiac creatine kinase in the coronary effluent and in the content of tumor necrosis factor-a TNF-a.in myocardial tissues. However, ischemic preconditioninghree cycles of 5-min ischemia and 5-min reperfusion.or pretreatment with CGRP for 5 min dramatically improved the recovery of cardiac function, and reduced the release of cardiac creatine kinase and the TNF-a content. The effect of ischemic preconditioning was abolished by CGRP-8-37., the selective CGRP receptor antagonist, and by capsaicin, which depletes sensory nerve neurotransmitter content, but was unaltered by treatment with glibenclamide, a blocker of the ATP-sensitive potassiumKATP.channel. The protective effects of exogenous CGRP-induced preconditioning were also not blocked by glibenclamide. These results suggest that the cardioprotective effects afforded by CGRP-mediated ischemic preconditioning are related to inhibition of cardiac TNF-a production, but not to activation of the KATP channel.
Preconditioning, CGRPcalcitonin gene-related peptide., , TNF-a tumor necrosis factor-a., , libenclamide, Heart,, rat
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