李胜男
致力于心血管系统疾病药物靶标的探索。
个性化签名
- 姓名:李胜男
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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:致力于心血管系统疾病药物靶标的探索。
李胜男,女,特聘教授,博士生导师。1989年在中国医科大学获得硕士学位,1999年在德国 Dresden技术大学药理毒理所获得博士学位。后继续于新加坡国立大学进行博士后研究。现任南京医科大学教授、博士生导师、卫生部抗体技术重点实验室副主任,兼中国药理学会会员、江苏省药理学会常务理事、南京市药学会理事、南京医科大学学报(英文版)编委等学术职务。致力于心血管系统疾病药物靶标的探索。阐述新型多肽urocortin对心血管系统的作用,发现该肽可保护心脏、减少缺血再灌注损伤导致的心肌梗塞面积、抑制心脏与血管的重构。发表SCI收录论文20余篇。主持国家自然科学基金、教育部重点项目、留学回国人员基金课题及江苏省级课题多项。指导博士、硕士研究生9名。2005年参加改编《Basic and clinical Pharmacology》(科学出版社)、主编高等教育出版社全日制医学规划教材《药理学》,2004年主编《Fundamental Medical Pharmacology》(吉林科技出版社)、编著《心血管药理新论》(科学出版社)。
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273
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成果数
8
【期刊论文】Breakthroughs and Views Urocortin: A cardiac protective peptide?
李胜男, Jin Tao, Shengnan Li*
Biochemical and Biophysical Research Communications 332(2005)923~926,-0001,():
-1年11月30日
Urocortin(UCN),a member of the corticotropin-releasing hormone(CRH)-related peptides,has been reported to play biologically diverse roles in several systems such as cardiovascular, reproductive, appetite, stress, inflammatory responses, etc. In heart, it was reported to have protective effects.On the other hand,it was also reported to have cardiac inotropic and hypertrophic effects and hence to cause cardiac remodeling.This paper will review the effects of UCN in cardiac system.
Urocortin, Corticotropin-releasing hormone, Ischemic preconditioning, ATP-sensitive potassium channels
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【期刊论文】Effects of urocortin on T-type calcium currents in mouse spermatogenic cells
李胜男, Jin Tao, Yuqing Wu, Jie Chen, Hui Zhu, Shengnan Li*
Biochemical and Biophysical Research Communications 329(2005)743~748,-0001,():
-1年11月30日
Urocortin(UCN),a newly isolated peptide,has been found to play an important role mainly in female reproductive system.In order to investigate the effect of UCN on T-type calcium currents(ICa,T), exploring the mechanisms of UCN s role in male reproductive system,especially in acrosome reaction,we directly measured the ICa,T in mouse spermatogenic cells exposed to UCN using standard whole-cell patch clamp recording technique.Our results showed that UCN reversibly inhibited the T-type Ca2+ currents in the cells in a concentration-dependent manner.The current density was inhibited by about 19% after exposure of the cells to UCN(0.1 lM)for 5 min,from the control value of 6.75±1.17 to 5.26±0.82 pA/pF.UCN up-shifted the current-voltage(I-V)curve.Frequency-dependence of UCN’s effects on ICa,T was also observed.Moreover,UCN at 0.1 lM did not markedly affect the activation of ICa,T but shifted the inactivation curve of ICa,T to the left.The inhibitory effect of UCN on the T-type Ca2+ current was not affected by Astressin,the CRF receptor blocker.Since T-type calcium channels are a key component in acrosome reaction,our data suggest that UCN might be a significant factor in male reproductive action and a potential contraceptive agent.
Urocortin, T-type calcium channel, Patch-clamp, Spermatogenic cells, Acrosome reaction
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李胜男, Jin Tao, Jiandong Chen, Yuqing Wu, Shengnan Li ∗
Peptides 26(2005)2239~2245,-0001,():
-1年11月30日
The newly isolated peptide,urocortin(UCN),is a member of the corticotropin-releasing factor(CRF)-related peptides that has been found to have potent cardiovascular protective effects.In order to investigate the effect of UCN on the viability of adult rat vascular smooth muscle cells(VSMC)and the relevant mechanisms,we exposed the VSMC to UCN to observe the change in cell viability using MTT assay and intracellular calcium concentration using confocal laser scanning microscope methods.Our results showed that UCN(10−7M)inhibited the viability of VSMC by about 26% (P<0.05, compared to control).The effect was concentration-dependent, but it was not dependent on the affecting time.Glybenclamide (Gly, 10−5M), the ATP-sensitive potassium channel(KATP channel)blocker,and astressin (10−6 M), a competitive antagonist of CRF receptors,had no influence on this inhibition.Bay K8644 (10−6 M), a special L-type calcium channel activator,increased the viability of VSMC. Pre-treatment of the cells with UCN diminished the effect of Bay K8644 (n=6, P<0.05). UCN was also observed to reduce the intracellular Ca2+ increase induced by KCl and Bay K8644. There was no significant difference in nitrite accumulation between UCN groups and the control.In conclusion,UCN reduced the viability of VSMC through L-type calcium channels.These interesting results might suggest that UCN may be a new vasoactive agent involved in hindering vascular remodeling in combination with previous reports about UCN's hypotensive effects.
Urocortin, Calcium channel, Vascular smooth muscle cells, Cell viability, Vascular remodeling
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【期刊论文】Breakthroughs and Views Effects of urocortin via ion mechanisms or CRF receptors?
李胜男, Jin Tao a, b, Shengnan Li b, *
Biochemical and Biophysical Research Communications 336(2005)731~736,-0001,():
-1年11月30日
Urocortin(UCN),a newly isolated peptide related to hypothalamic corticotrophin releasing factor(CRF)family,had been reported to play biologically diverse roles in several systems such as cardiovascular,reproductive,appetite,stress,and inflammatory responses,etc.It was thought previously to be an endogenous agonist,producing the several actions previously attributed to CRF. But, recently, it was shown to directly reduce L-type calcium currents of acute isolated cardiac myocytes and T-type calcium currents in mouse spermatogenic cells via inhibiting calcium channel instead of binding first to its CRF-R2 receptors.UCN could also reduce the intracellular calcium in vascular smooth muscle cells via inhibiting calcium channel directly.Furthermore,UCN could increase the gene expression of ATP-sensitive potassium channels(KATP)and activate sarcolemmal ATP-sensitive potassium current during normal or hypoxia,which could be inhibited by glibenclamide,a specific KATP blocker.This review will highlight the current novel findings on the ionic mechanisms by which UCN may exert its several actions.
Urocortin, Corticotrophin releasing factor, Calcium channels, ATP-sensitive potassium channels
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【期刊论文】Effects of SNP, GLU and GABA on the neuronal activity of striatum nucleus in rats
李胜男, Chun-Na Liu a, Xinyu Liu b, Dongming Gaob, Shengnan Li a, ∗
Pharmacological Research 51(2005)547~551,-0001,():
-1年11月30日
This study investigated the activity of nitric oxide(NO)in the striatum(STR)for a further comprehension of the pathogenesis of Parkinson’s disease(PD).Microiontophoresis was used to observe the effects of sodium nitroprusside(SNP),l-glutamic acid(GLU)and γ-aminobutyric acid(GABA)on STR neurons’ firing rates.Itwas observed that 77.27%(51/66)of the tested STR neurons were excited by SNP.This excitatory effect could be antagonized by theNOsynthase(NOS)inhibitor,N(G)-nitro-l-arginine methyl ester(l-NAME).During the microiontophoresis of GLU,the excitatory firing of STR neurons was also attenuated by addition of l-NAME while SNP application could enhance the excitation of the neurons.On the other hand,in the presence of GABA,SNP still excited the tested STR neurons.These results demonstrated that NOergic,GLUergic and GABAergic co-existed in the same STR neurons.NOergic and GLUergic were excitatory whereas GABAergic was inhibitory on the firing activity in STR neurons.
Microelectrophoresis, Striatum, Nitric oxide, Sodium nitroprusside, l-Glutamic acid, γ-Aminobutyric acid
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【期刊论文】Effect of urocortin on L-type calcium currents in adult rat ventricular myocytes
李胜男, Jin Tao, Hua’e Xu, Cui Yang, Chun-Na Liu, Shengnan Li∗
Pharmacological Research 50(2004)471~476,-0001,():
-1年11月30日
The newly isolated peptide,urocortin(UCN)has been found to have potent cardioprotective effects.In order to investigate the effectof UCN on L-type calcium currents(ICa,L),exploring the mechanisms of UCN’s cardioprotective effects,we directly measured the ICa,Lin the adult rat cardiac myocytes exposed to UCN using standard whole-cell patch-clamp recording technique.Our results showed that UCN exerted decreasing effects on the ICa,L of the single adult rat cardiac myocytes.The current density was inhibited by about 35% after exposure of the cells to UCN(0.1 mol L−1)for 10 min,from the control value of 7.19±1.44 pA/pF to 4.74±0.75 pA/pF(n=5,P<0.05).This ICa,L-inhibiting action of UCN was concentration dependent.Moreover,no frequency dependence of UCN effects on ICa,L was observed.In combination with previous reports,our results suggest that there might be a close relationship between the cardioprotective effects of UCN and L-type calcium channels.
Urocortin (, UCN), , Calcium channel, Patch-clamp, Ventricular myocyte
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李胜男, Shengnan Li, Marianne Blaschke, J
European Journal of Pharmacology 418(2001)7~14,-0001,():
-1年11月30日
Azelastine is used for symptomatic relief of allergic rhinitis and asthma bronchiale.In vitro studies in smooth muscle cells from guinea pig trachea and ileum demonstrate that the drug blocks L-type Ca2+ current(Ica,L)However,for safety reasons,it is important to know whether azelastine also affects cardiac ICa,L in therapeutically relevant concentrations.We have therefore studied the effects of azelastine on ICa,L in guinea pig ventricular myocytes using standard whole-cell patch-clamp technique.Force of contraction and action potentials from isolated papillary muscles of the same species were also investigated at physiological temperature(36℃)..Azelastine (30µM).significantly reduced force of contraction,shortened action potential duration,and depressed maximum upstroke velocity.ICa,L was elicited by 200-ms-long clamp steps fromy -100 to 0 mV(one pulse every3s).Azelastine blocked ICa,L reversibly and concentration-dependently with an IC50 of 20.2±1.3µM and a Hill coefficient of 1.1.At 10µM,azelastine shifted steady-state inactivation by 5 mV Žns7.to more negative potentials.The time course of ICa,L inactivation could be described by a double exponential function.Azelastine(10µM)significantly shortened the slow inactivation time constant(Ts) from 54.2±2.8 ms under control conditions to 38.7±2.9 ms(n=16)in the presence of drug.Azelastine also reduced low-voltage-activated Ca2+ currents with a similar IC50 value(24µM,at-35mV).Since the therapeutic plasma concentrations are in the order of 10–100 nM,we conclude that azelastine does indeed affect also cardiac ICa,L,but the concentrations required are at least two orders of magnitude larger than those obtained during drug therapy.q2001 Elsevier Science B.V.All rights reserved.
Azelastine, Action potential, Ca2+, current,, L-type, Ca2+, channel, Naq channel, Papillary muscle, Myocyte
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李胜男, Yu-Qing Wu a, Cheng-Hua Zhou b, Jin Tao a, Sheng-Nan Li a, *
Life Sciences 78(2006)2689~2696,-0001,():
-1年11月30日
Eosinophils are known to be the important effector cells in asthmatic airway inflammation.The purpose of this study was to investigate the effects of nobiletin,a polymethoxyflavonoid,on eosinophilic airway inflammation of asthmatic rats,and explore its possible mechanisms.Animals were actively sensitized by subcutaneous injection of ovalbumin(OVA).The inflammation in lung tissues of asthmatic rats was observed by hematoxylin and eosin(HE)staining.The eosinophils in blood and BALF were separated by Percoll density gradient centrifugation and counted under microscope.The level of Eotaxin was detected by enzyme-linked immunosorbent assay(ELISA).In addition,the apoptosis of eosinophils was labeled by TdT-mediated dUTP nick end labeling(TUNEL)technique,the semi-quantitative detection for Fas mRNA expression of eosinophils was performed by reverse transcription-polymerase chain reaction(RT-PCR).The airway inflammation of asthmatic rats pretreated with nobiletin was obviously alleviated.Nobiletin(1.5 and 5.0 mg/kg given intraperitoneally)significantly reduced OVA-induced increases in eosinophils,remarkably lowered the level of Eotaxin in blood and broncho-alveolar lavage fluid(BALF)of asthmatic rats.On the other hand,semi-quantitative RT-PCR analysis for Fas of eosinophils from OVA aerosol-challenged sensitized rats showed that Fas mRNA expression of eosinophils was obviously enhanced by nobiletin.Meanwhile,the apoptosis index of cultured eosinophils was significantly elevated after treatment with different doses of nobiletin.These results indicated that nobiletin could inhibit the eosinophilic airway inflammation.Lowering the levels of Eotaxin,relieving airway infiltration of eosinophils and promoting apoptosis of eosinophils by enhancing expression of Fas mRNA may be important mechanisms for nobiletin to antagonize eosinophilic airway inflammation of asthmatic rats.D 2005 Elsevier Inc.All rights reserved.
Nobiletin, Asthma, Airway inflammation, Eosinophil, Eotaxin, Fas, Apoptosis
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