吴春福
主要从事中枢神经药理学的研究
个性化签名
- 姓名:吴春福
- 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:主要从事中枢神经药理学的研究
吴春福,1982年以优秀成绩毕业于沈阳药学院,留校任教。1992年、1994年分别两次破格晋升为副教授、教授,1996年被评为博士生导师。1996年任沈阳药科大学常务副校长,2000年任校长。2000年获日本北海道药科大学博士学位。
1985年由国家公派赴意大利进修神经药理学,在国际上率先建立了应用脑内透析技术测定清醒动物脑内神经递质乙酰胆碱释放的方法,并应用此技术研究了药物和衰老对乙酰胆碱释放的影响,获"药理学研究专家"证书。1987年回国后,建立了神经药理研究实验室。
目前吴春福教授主要从事中枢神经药理学的研究。在药物对乙醇引起大鼠抗坏血酸释放影响的机制研究中有许多新发现,对于深入理解乙醇的中枢作用机理及研究滥用药物引起的中枢神经损伤的防治具有一定的指导意义。同时首次发现拟人参皂苷F11有抗吗啡成瘾和抗吗啡耐受性作用。目前正利用这些化合物,采取半合成或生物代谢的方法设计制备其他人参皂苷类成分,为研究开发可望有效抑制阿片类依赖性和耐受性的新药奠定化学和药理学基础。已申请了相关化合物的制备、临床新用途等3项专利,并获得发明专利一项。
近年来先后主持了科技部十五新药研究重大项目、自然科学基金、教育部青年骨干教师基金、国家新药基金、国家医药局青年基金以及辽宁省自然科学基金、技术基金等重大课题的研究,并主编出版了《现代老年药学》、《药学概论》和参加编著了《药理实验方法学》、《中医方剂的药理与应用》、《中药药理研究方法学》等多部学术著作。
在教学方面,为本科生和研究生开设讲授《中药药理学》、《专业英语》、《药学概论》、《分子药理学》、《神经生物学进展》等课程。近年来已培养研究生40余人,博士后5人,其中已毕业硕士生18人,博士生19人。至今在国内外期刊共发表学术论文近150篇,其中SCI收录60余篇。
参加工作以来, 在科研教学方面获得许多奖项。2006年入选度“辽宁省高等学校优秀人才支持计划”,2006年获得沈阳市科技创新奖,2005年获沈阳市科技振兴奖,2004年被评为新世纪百千万人才工程国家级人选,获第六届沈阳市优秀科技工作者奖,2002年获得卫生部颁发的吴阶平保罗•杨森医学药学研究二等奖等。兼任国家新药研究与开发专家委员会委员、中国药理学会理事、中国药理学会中药药理专业委员会委员、中国药学会常务理事、中国药学会老年药学委员会副主任委员、国家新药评审委员会委员、中国医学教育学会理事、中国医药教育协会药学院校委员会副理事长、辽宁省药学会理事长等。
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成果数
20
吴春福, Gong Cheng Zuo, Jing Yu Yang, Yue Hao, Ying Xu Dong, Chun Fu Wu
G. C. Zuo et al. Toxicology Letters 169 (2007) 253-258,-0001,():
-1年11月30日
It is controversial regarding to the roles of acetaldehyde and ethanol in the central nervous system. In the present study, the effects of acetaldehyde and ethanol on extracellular levels of glutamate, taurine and GABA in the anterior cingulate cortex (ACC) of freely moving rats were investigated by using the microdialysis technique coupled to high performance liquid chromatography (HPLC) with fluorescent detection. The result showed that glutamate levels were significantly decreased after acute administration of acetaldehyde (AcH, 20 and 100mg/kg, i.p.), while taurine levels were significantly increased after the higher dose of acetaldehyde (100mg/kg, i.p.). GABA levels had no changes at any doses of acetaldehyde tested. Interestingly, similar changes of these amino acids were induced by ethanol (EtOH, 3g/kg, i.p.) when sodium azide (NaN3, 10mg/kg, i.p.), a catalase inhibitor that can reduce brain ethanol metabolism, was used simultaneously. These findings suggest that acetaldehyde and ethanol have the similar effects on the extracellular output of glutamate, taurine and GABA in the ACC.
Acetaldehyde, Ethanol, Glutamate, Taurine, GABA, Anterior cingulate cortex
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吴春福, Yue Hou, , Chun Fu Wu, Jing Yu Yang, Tao Guo
Y. Hou et al. Progress in Neuro-Psychopharmacology & Biological Psychiarty xx (2006) xxx-xxx,-0001,():
-1年11月30日
Many schizophrenic patients exhibit impairments in neurocognitive functions. Typical antipsychotic drugs such as haloperidol, have limited or even detrimental influence on cognitive functions. In contrast, atypical antipsychotic drugs, such as clozapine and olanzapine, may improve memory function in schizophrenics. However, only a few studies have been conducted to directly compare the effects of olanzapine, clozapine and haloperidol on memory functions in animal models. Thus, their effects on this issue were investigated in the present studies by using one-way step-through passive avoidance task and Morris water maze as models of learning and memory. The results showed that olanzapine did not affect acquisition, consolidation or retrieval process in step-through test. Moreover, it improved spatial learning function in mice in Morris water maze task. Clozapine and haloperidol appeared to impair acquisition process and consolidation process, respectively, in step-through test. Both drugs impaired spatial learning function in mice in Morris water maze task. The results suggested a positive implication for the clinical medication of olanzapine in schizophrenic treatment.
Clozapine, Haloperidol, Memory, Morris water maze, Olanzapine, Step-through test
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吴春福, ue Hou, , Chun Fu Wu, Jing Yu Yang, Xiang He, Xiu Li Bi, Liang Yu, Tao Guo
Y. Hou et al. Progress in Neuro-Psychopharmacology & Biological Psychiatry xx (2006) xxx-xxx,-0001,():
-1年11月30日
Schizophrenia is a devastating illness of unknown etiology and the basis for its treatment rests in the symptomatic response to antipsychotics. It was found that some of the patients with schizophrenia elicited microglia activation. The present study used lipopolysaccharide (LPS)-activated mouse microglial cell line N9 as an in vitro model to mimic microglia activation seen in the patients with schizophrenia. The effects of clozapine, olanzapine and haloperidol on the release of nitric oxide (NO) by LPS-stimulated N9 cells were investigated. The results showed that olanzapine significantly inhibited NO release by LPS-stimulated N9 cells. Clozapine and haloperidol did not show significant effects on this model. The present study suggested that the inhibiting effect of olanzapine on the NO release by LPS-stimulated microglial cells might be a new mechanism through which olanzapine exhibits its therapeutic effect in the treatment of schizophrenia.
Clozapine, Haloperidol, N9 cells, Nitric oxide (, NO), , Olanzapine
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吴春福, Fang Dai, Jing Yu Yang, Pei Fei Gu, Yue Hou, Chun Fu Wu
BRAINRESEARCH 1125 (2006) 163-170,-0001,():
-1年11月30日
The mechanism of ethanol, morphine, methamphetamine (MAP), and nicotine-induced ascorbic acid (AA) release in striatum, and nucleus accumbens (NAc) is not well understood. Our previous study showed that the glutamatergic system was involved in the addictive drug-induced AA release in NAc and striatum. Furthermore, frontal decortication eliminates drug-induced ascorbic acid release in the striatum but not in the NAc. In the present study, the roles of the hippocampus in drug-induced AA release in the striatum and NAc were studied by using microdialysis coupled to high performance liquid chromatography with electrochemical detection (HPLC-ECD). Ethanol (3.0 g/kg, i.p.), methamphetamine (3.0 mg/kg, i.p.), and nicotine (1.5 mg/kg, i.p.) significantly stimulated AA release in the striatum and NAc, respectively. Morphine (20 mg/kg, i.p.) significantly stimulated AA release in the striatum, but not in the NAc. After hippocampal lesion by kainic acid, AA release induced by ethanol, methamphetamine, and nicotine could be eliminated in NAc, but not in the striatum. These results suggest that the hippocampus might be a common and necessary area in addictive drug-induced AA release in the NAc, which also imply that different pathways might be involved in drug-induced AA release in the striatum and the NAc of the rats.
Ascorbic acid,, Striatum,, Nucleus accumben,, Ethanol,, Morphine,, Methamphetamine
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吴春福, Yan ZHANG, , Wan-Ping LAI, Ping-Chung LEUNG, Chun-Fu WU, Xin-Sheng YAO, and Man-Sau WONG
Biol. Pharm. Bull. 29 (2) 291-296 (February 2006),-0001,():
-1年11月30日
The aim of this study was to evaluate the effect of Fructus Ligustri Lucidi (FLL), a kidney-tonifying Chinese herbal medicine, on the biochemical markers of bone turnover, calcium metabolism and balance in osteoporotic rat model developed by ovariectomy. Four weeks after surgical operation, animals were randomly assigned to one of the four treatments for 14 weeks: sham-operated control treated with vehicle (sham, n=8), ovariectomized group treated with vehicle (OVX, n=8), OVX group treated with 17β-estradiol (E2, n=10, 2μg/kg/d) and OVX group treated with FLL extracts (FLL, n=10, 550mg/kg/d). Serum osteocalcin and urinary deoxypyridinoline levels were upregulated in rats in response to OVX, suggesting that the bone turnover rate was accelerated in these animals. Treatment of OVX rats with FLL extract could prevent OVX-induced increase in bone turnover by suppression of both serum osteocalcin (p<0.05, vs. OVX) and urinary deoxypyridinoline (p<0.05, vs. OVX) levels. In addition, FLL extract could prevent OVX-induced loss of calcium in rats by increasing the intestinal calcium absorption rate (p<0.01, vs. OVX), suppressing urinary Ca excretion (p<0.05, vs. OVX) as well as increasing bone calcium content (p<0.05, vs. OVX). Our study is the first to report that FLL can modulate bone turnover and calcium balance in OVX rats and it might be a potential candidate for prevention and treatment of postmenopausal osteoporosis.
Fructus Ligustri Lucidi, ovariectomy, bone turnover, calcium balance
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吴春福, Pei Fei Gu, Chun Fu Wu, Jing Yu Yang, Yu Shang, Yue Hou, Xiu Li Bi, Fang Dai
P. F. Gu et al. Neuroscience Letters 399 (2006) 79-84,-0001,():
-1年11月30日
Previous studies have shown that striatumand nucleus accumbens (NAc) are two different structures inmediating addictive drug-induced ascorbic acid (AA) release. In order to further characterize the different effects of drugs-induced AA release in the striatum and NAc, in the present study, we investigated the effect of ethanol, morphine, methamphetamine, nicotine-induced AA release in these two nuclei using microdialysis coupled to high performance liquid chromatography with electrochemical detection (HPLC-ECD). All drugs were continuously perfused directly into the striatum or NAc. This study showed that local intrastriatal or intra-accumbensal perfusion of ethanol (500 μM) could increase AA release to 280, 260% in the striatum and NAc, respectively. Intra-striatal infusion of morphine (1mM), methamphetamine (250 μM) or nicotine (500 μM), reduce striatal AA release to 48, 50, 45%, respectively. While given intra-accumbensally, morphine (1mM), methamphetamine (250 μM) or nicotine (500 μM) increase AA release to 165, 160, 160%, respectively. These results suggested that different presynaptic or postsynaptic mechanisms might be involved in addictive drug-induced AA release in the striatum and NAc.
Addictive drugs, Ascorbic acid, Striatum, Nucleus accumbens, Microdialysis
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吴春福, Chun-Li Li, Jing-Hai Zhang, Bao-Feng Yang, Jun-Dong Jiao, Ling Wang, Chun-Fu Wu
C. -L. Li et al. Regulatory Peptides 133 (2006) 74-81,-0001,():
-1年11月30日
A new recombinant neurotoxic polypeptide ANEPIII (BmK ANEPIII) derived from Scorpion peptide, which was demonstrated with antineuroexcitation properties in animal models, was examined for its action on K+ currents in primary cultured rat hippocampal and cortical neurons using the patch clamp technique in the whole-cell configuration. The delayed rectifier K+ current (Ik) was inhibited by externally applied recombinant BmK ANEPIII, while the transient A-current (IA) remained virtually unaffected. BmK ANEPIII 3 μM, reduced the delayed rectifier current by 28.2% and 23.6% in cultured rat hippocampal and cortical neurons, respectively. The concentration of half-maximal block was 155.1 nM for hippocampal neurons and 227.2 nM for cortical neurons, respectively. These results suggest that BmK ANEPIII affect K+ currents, which may lead to a reduction in neuronal excitability.
Recombinant neurotoxic polypeptide, Anticonvulsant, Potassium channel, Hippocampus, Cortex, Whole-cell clamp patch
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吴春福, Yue Hao, Jing Yu Yang, Ming Guo, Chun Fu Wu, Min Fan Wu
Y. Hao et al. Brain Research 1040 (2005) 191-196,-0001,():
-1年11月30日
In the present study, we investigated the effect of morphine on the extracellular levels of glutamate in the anterior cingulate cortex (ACC) in freely moving rats using in vivo microdialysis coupled to high performance liquid chromatography and electrochemical detection. The results showed that either acute or chronic morphine treatment decreased the extracellular levels of glutamate in the ACC. Naloxone could reverse the decrease induced by chronic morphine treatment. The present study provided the first neurochemical evidence that morphine decreased extracellular levels of glutamate in the ACC, suggesting that glutamate in ACC is involved in the central actions of morphine.
Morphine, Glutamate, Anterior cingulate cortex, Microdialysis
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吴春福, Pei Fei Gu, Jing Yu Yang, Chun Fu Wu, Wei Li, Yu Shang
P. F. Gu et al. Brain Research 1033 (2005) 194-201,-0001,():
-1年11月30日
The mechanism of morphine-, methamphetamine-, and nicotine-induced ascorbic acid (AA) release in the striatum and nucleus accumbens (NAc) is not well understood. In the present study, the roles of the corticostriatal and corticoaccumbens pathways in drug-induced AA release were studied by using microdialysis coupled to high performance liquid chromatography with electrochemical detection (HPLC-ECD). The results showed that morphine (20 mg/kg), methamphetamine (3.0 mg/kg), or nicotine (1.5 mg/kg) intraperitoneally (i.p.) significantly stimulated AA release in the striatum to more than 180%, 190%, and 140% compared with saline groups, respectively. These effects could be completely eliminated by frontal decortication, or antagonized by MK-801 (1.0 mg/kg). Moreover, methamphetamine or nicotine also significantly induced AA release in the NAc to more than 180% and 150% compared with saline groups, respectively. However, these effects could not be eliminated by frontal decortication. Although the effects of methamphetamine or nicotine in the NAc could be antagonized by MK-801, two-way ANOVA analysis did not show a significantly interaction between MK-801 and methamphetamine, or nicotine. The results indicates that the corticostriatal glutamatergic pathway may be a common and necessary pathway in drug-induced AA release in the striatum, but the corticoaccumbens glutamatergic pathway may not be crucial in drug-induced AA release in the NAc. The present study implies that different mechanisms might be involved in drug-induced AA release in the striatum and the NAc in rats.
Ascorbic acid, Striatum, Nucleus accumbens, Morphine, Methamphetamine, Nicotine
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吴春福, Xiu Li Bi, Jing Yu Yang, Ying Xu Dong, Ji Ming Wang, Yong Hong Cui, Takashi Ikeshima, Yu Qing Zhao, Chun Fu Wu
X. L. Bi et al. International Immunopharmacology 5 (2005) 185-193,-0001,():
-1年11月30日
Upon activation, brain macrophages, the microglia, release proinflammatory mediators that play important roles in eliciting neuroinflammatory responses associated with neurodegenerative diseases. As resveratrol, an antioxidant component of grape, has been reported to exert anti-inflammatory activities on macrophages, we investigated its effects on the production of TNF-alpha (TNF-α) and nitric oxide (NO) by lipopolysaccharide (LPS)-activated microglia. Exposure of cultured rat cortical microglia and a mouse microglial cell line N9 to LPS increased their release of TNF-α and NO, which was significantly inhibited by resveratrol. Further studies revealed that resveratrol suppressed LPS-induced degradation of IκBα, expression of iNOS and phosphorylation of p38 mitogen-activated protein kinases (MAPKs) in N9 microglial cells. These results demonstrate a potent suppressive effect of resveratrol on proinflammatory responses of microglia, suggesting a therapeutic potential for this compound in neurodegenerative diseases accompanied by microglial activation.
Resveratrol, Microglia, NO, TNF-α, IκBα, p38
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