王晓民
主要从事针刺镇痛、帕金森病、阿尔茨海默病防治研究。
个性化签名
- 姓名:王晓民
- 目前身份:
- 担任导师情况:
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学术头衔:
博士生导师, 教育部“新世纪优秀人才支持计划”入选者
- 职称:-
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学科领域:
神经病学
- 研究兴趣:主要从事针刺镇痛、帕金森病、阿尔茨海默病防治研究。
1956年3月生,男,1982年于中国医科大学获医学学士,1988年于大连医科大学获医学硕士,1993年获医学博士(北京医科大学与德国慕尼黑大学联合培养4年)。自1993起,先后任北京医科大学副教授、教授、博士生导师。曾任北京大学基础医学院常务副院长、教育部及卫生部神经科学重点实验室副主任、北京大学神经科学研究所副所长及北京大学基础医学院神经生物学系副主任。现任首都医科大学副校长;兼任中国神经科学学会副理事长,中国生理学会秘书长及神经科学专业委员会主任委员,北京神经科学学会理事长等职。现任《中华神经医学杂志》副主编,《基础医学与临床》副主编等数种杂志编委会常务编委或委员。
自1985年以来主要从事针刺镇痛、帕金森病、阿尔茨海默病防治研究。先后主持部委级以上科研项目十六项;在国内外发表论文80余篇(SCI收录26篇);主编著作两部,参编著作6部;研究成果获部级奖五项(二等奖3项、三等奖2项)。获国际专利申请号一项,国内专利一项和专利申请号一项;曾先后赴德国慕尼黑大学、美国洛克菲勒大学、美国印第安那大学和美国冷泉港实验室任客座研究员或访问科学家,进行合作科研。
1993年获“首届全国中青年医学科技之星”称号;1994年入选“国家教委跨世纪优秀人才计划”;1998年获美国中华医学基金会优秀青年学术骨干奖;1999年获国务院颁发的政府特殊津贴。现任国家973、863和北京市自然科学基金委重点项目等有关“帕金森病的发病机制和防治基础”研究的负责人。
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成果数
10
王晓民, Xi-Bin Liang, Xian-Yu Liu, Feng-Qiao Li, Yong Luo, Jun Lu, Wang-MingZhang, Xiao-Min Wang, Ji-Sheng Han
Molecular Brain Research 108 (2002) 51-59,-0001,():
-1年11月30日
Electroacupuncture (EA) has been used in China for many years to treat Parkinson’s disease (PD) with reportedly effective results. However, the physiological and biological mechanism behind its effectiveness is still unknown. In the present study, different frequencies of chronic EA stimulation (0, 2, 100 Hz) were tested in a partially lesioned rat model of PD which was induced by transection of the medial forebrain bundle (MFB). After 24 sessions of EA stimulation (28 days after MFB transection), dopaminergic neurons in the ventral midbrain were examined by immunohistochemical staining, and brain-derived neurotrophic factor (BDNF) mRNA levels in ventral midbrain were measured by in situ hybridization. The results show a marked decrease of dopaminergic neurons on the lesioned side of the substantia nigra (SN) comparing with the unlesioned side. Zero Hz and 2 Hz EA stimulation had no effect on the disappearance of dopaminergic neurons. However, after 100 Hz EA, about 60% of the tyrosine hydroxylase (TH)-positive neurons remained on the lesioned side of the SN. In addition, levels of BDNF mRNA in the SN and ventral tegmental area (VTA) of the lesioned side were significantly increased in the 100 Hz EA group, but unchanged in the 0 and 2 Hz groups. Our results suggest that long-term high-frequency EA is effective in halting the degeneration of dopaminergic neurons in the SN and up-regulating the levels of BDNF mRNA in the subfields of the ventral midbrain. Activation of endogenous neurotrophins by EA may be involved in the regeneration of the injured dopaminergic neurons, which may underlie the effectiveness of EA in the treatment of PD.
Parkinson’s disease, Electroacupuncture, Brain-derived neurotrophic factor, Regeneration, Rat
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【期刊论文】Triptolide inhibitsTNF-a, IL-1
王晓民, Hui-Fang Zhou, Dong-Bin Niu, Bing Xue, Feng-Qiao Li, Xian-Yu Liu, Qi-Hua He, Xin-Hong Wang and Xiao-Min WangCA
Lippincott Williams & Wilkins Vol. 14, No. 7, 23 May 2003,-0001,():
-1年11月30日
Microglia are believed to participate in the mediation of neurodegeneration through producing a variety of cytotoxic factors upon activation. Pharmacological intervention inmicroglial activation may therefore exert a neuroprotective effect. In exploring pharmacological agents that can effect microglial activation, we found in this study that triptolide possesses a powerful inhibitory influence over microglia. Pretreatment with triptolide was able to dose-dependently reduce the lipopolysaccharide (LPS)-induced nitrite accumulation and tumor necrosis factor-a and interleukin-1
Inflammation, Microglia, Neuroprotection, Nitric oxide, Proinflammatory cytokines, Triptolide, Tripterygiumwilfordii Hook F.,
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王晓民, Xian-Yu Liu, a Hui-Fang Zhou, a Yan-Li Pan, a Xi-Bin Liang, a Dong-Bin Niu, a Bing Xue, a Feng-Qiao Li, a Qi-Hua He, a Xin-Hong Wang, a and Xiao-Min Wang a, b, *
Experimental Neurology 189(2004)189-196,-0001,():
-1年11月30日
Through producing a variety of cytotoxic factors upon activation, microglia are believed to participate in the mediation ofneurodegeneration. Intervention against microglial activation may therefore exert a neuroprotective effect. Our previous study has shown thatthe electro-acupuncture (EA) stimulation at 100Hz can protect axotomized dopaminergic neurons from degeneration. To explore theunderlying mechanism, the effects of 100 Hz EA stimulation on medial forebrain bundle (MFB) axotomy-induced microglial activation wereinvestigated. Complement receptor 3 (CR3) immunohistochemical staining revealed that 24 sessions of 100Hz EA stimulation (28 days afterMFB transection) significantly inhibited the activation of microglia in the substantia nigra pars compacta (SNpc) induced by MFBtransection. Moreover, 100 Hz EA stimulation obviously inhibited the upregulation of the levels of tumor necrosis factor (TNF)-a andinterleukin (IL)-1h mRNA in the ventral midbrains in MFB-transected rats, as revealed by reverse transcriptase polymerase chain reaction(RT-PCR). ED1 immunohistochemical staining showed that a large number of macrophages appeared in the substantia nigra (SN) 14 daysafter MFB transection. The number of macrophages decreased by 47% in the rats that received 12 sessions of EA simulation after MFBtransection. These data indicate that the neuroprotective role of 100Hz EA stimulation on dopaminergic neurons in MFB-transected rats islikely to be mediated by suppressing axotomy-induced inflammatory responses. Taken together with our previous results, this study suggeststhat the neuroprotective effect of EA on the dopaminergic neurons may stem from the collaboration of its anti-inflammatory and neurotrophicactions.D 2004 Elsevier Inc. All rights reserved.
Electro-acupuncture, Microglia, Inflammation, Proinflammatory cytokines, Neuroprotection, Axotomy
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王晓民, Xuan Wang a, , Yanyan Lub, Huanqing Zhang b, Kun Wang a, Qihua Hea, b, Yue Wang a, Xianyu Liu a, Linsong Li b, Xiaomin Wang a, c, ∗
Int. J. Devl Neuroscience 22(2004)175-183,-0001,():
-1年11月30日
Neural progenitor cells have shown the effectiveness in the treatment of Parkinson's disease, but the therapeutic efficacy remains variable. One of important factors that determine the efficacy is the necessity of pre-differentiation of progenitor cells into dopaminergic neuronsbefore transplantation. This study therefore investigated the therapeutic efficacy of mesencephalon-derived human neural progenitor cellswith or without the pre-differentiation in alleviating a rat model of Parkinson's disease.We found that a combination of 50ng/ml fibroblastgrowth factor 8, 10ng/ml glial cell line-derived neurotrophic factor and 10M forskolin facilitated the differentiation of human fetalmesencephalic progenitor cells into dopaminergic neurons in vitro. More importantly, after transplanted into the striatum of parkinsonianrats, only pre-differentiated grafts resulted in an elevated production of dopamine in the transplanted site and the amelioration of behavioralimpairments of the parkinsonian rats. Unlike pre-differentiated progenitors, grafted intact progenitors rarely differentiated into dopaminergicneurons in vivo and emigrated actively away from the transplanted site.These data demonstrates the importance of pre-differentiation of human progenitor cells before transplantation in enhancing therapeuticpotency for Parkinson's disease.
Neural progenitor cells, Parkinson', s disease, Cell differentiation, Cell transplantation, Migration, Dopaminergic neurons, Central nervous system
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王晓民, Kun Wang a, Jian-Jun Wang a, Yue Wang a, Qi-Hua Hea, Xuan Wang a, Xiao-Min Wang a, b, ∗
Neuroscience Letters 364(2004)154-158,-0001,():
-1年11月30日
This study investigated the proliferation and differentiation of adult neural progenitor cells (aNPCs) derived from the striatum and substantianigra (SN) of parkinsonian rats. We found that aNPCs isolated from the two areas of parkinsonian rats readily formed nestin-enrichedneurospheres in vitro and exhibited an ability to differentiate into either neurons or astrocytes. Injection of epidermal growth factor (EGF)and basic fibroblast growth factor (bFGF) into the striatum of parkinsonian rats prior to the harvesting striatal aNPCs significantly increasedthe neurosphere formation rate and multiple differentiation capacity of these aNPCs when cultured in vitro. These data suggest that striataland nigral adult NPCs in parkinsonian rats retain the abilities of proliferation and differentiation in vitro. In addition, exogenously appliedgrowth factors could up-regulate the developmental potential of aNPCs. We conclude that our data supports the notion that endogenous cellreplacement therapies may be useful for the future treatment of Parkinson’s disease (PD).
Adult neural progenitor cells, Neurospheres, Parkinson', s disease, Growth factors, Striatum, Substantia nigra
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王晓民, Xian-Yu Liu, a Hui-Fang Zhou, a Yan-Li Pan, a Xi-Bin Liang, a Dong-Bin Niu, a Bing Xue, a Feng-Qiao Li, a Qi-Hua He, a Xin-Hong Wang, a and Xiao-Min Wang a, b, *
Experimental Neurology 189(2004)189-196,-0001,():
-1年11月30日
Through producing a variety of cytotoxic factors upon activation, microglia are believed to participate in the mediation ofneurodegeneration. Intervention against microglial activation may therefore exert a neuroprotective effect. Our previous study has shown thatthe electro-acupuncture (EA) stimulation at 100 Hz can protect axotomized dopaminergic neurons from degeneration. To explore theunderlying mechanism, the effects of 100 Hz EA stimulation on medial forebrain bundle (MFB) axotomy-induced microglial activation wereinvestigated. Complement receptor 3 (CR3) immunohistochemical staining revealed that 24 sessions of 100 Hz EA stimulation (28 days afterMFB transection) significantly inhibited the activation of microglia in the substantia nigra pars compacta (SNpc) induced by MFBtransection. Moreover, 100 Hz EA stimulation obviously inhibited the upregulation of the levels of tumor necrosis factor (TNF)-a andinterleukin (IL)-1h mRNA in the ventral midbrains in MFB-transected rats, as revealed by reverse transcriptase polymerase chain reaction(RT-PCR). ED1 immunohistochemical staining showed that a large number of macrophages appeared in the substantia nigra (SN) 14 daysafter MFB transection. The number of macrophages decreased by 47% in the rats that received 12 sessions of EA simulation after MFBtransection. These data indicate that the neuroprotective role of 100 Hz EA stimulation on dopaminergic neurons in MFB-transected rats islikely to be mediated by suppressing axotomy-induced inflammatory responses. Taken together with our previous results, this study suggeststhat the neuroprotective effect of EA on the dopaminergic neurons may stem from the collaboration of its anti-inflammatory and neurotrophicactions.D 2004 Elsevier Inc. All rights reserved.
Electro-acupuncture, Microglia, Inflammation, Proinflammatory cytokines, Neuroprotection, Axotomy
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【期刊论文】Electro-acupuncture improves behavior and upregulates GDNF mRNA in MFB transected rats
王晓民, Xi-Bin Liang, Yong Luo, Xian-Yu Liu, Jun Lu, Feng-Qiao Li, Qian Wang, Xiao-Min WangCA and Ji-Sheng Han
Vol 14 No8 11 June 2003,-0001,():
-1年11月30日
Low and high frequency electro-acupuncture (EA) stimulationwas used in rats that had been lesioned by medial forebrain bundle transection. Behavioral tests showed that both low and high frequency EA stimulation signi
Electro-acupuncture, Glial cell-line-derived neurotrophic factor, Parkinson', s disease, Rat, Regeneration
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王晓民, Feng-Qiao Li, Xiu-Zhi Lu, Xi-Bin Liang, Hui-Fang Zhou, Bing Xue, Xian-Yu Liu, Dong-Bin Niu, Ji-Sheng Han, Xiao-Min Wang*
Journal of Neuroimmunology 148(2004)24-31,-0001,():
-1年11月30日
Mounting lines of evidence have suggested that brain inflammation participates in the pathogenesis of Parkinson's disease. Triptolide is oneof the major active components of Chinese herb Tripterygium wilfordii Hook F, which possesses potent anti-inflammatory andimmunosuppressive properties. We found that triptolide concentration-dependently attenuated the lipopolysaccharide (LPS)-induced decreasein [3H]dopamine uptake and loss of tyrosine hydroxylase-immunoreactive neurons in primary mesencephalic neuron/glia mixed culture.Triptolide also blocked LPS-induced activation of microglia and excessive production of TNFa and NO. Our data suggests that triptolide mayprotect dopaminergic neurons from LPS-induced injury and its efficiency in inhibiting microglia activation may underlie the mechanism.D 2003 Elsevier B.V. All rights reserved.
Triptolide, Tripterygium wilfordii Hook F, Inflammation, Microglia, Parkinson', s disease, Neurodegeneration
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王晓民, Feng-Qiao Li, Xiao-Xin Cheng, Xi-Bin Liang, Xin-Hong Wang, Bing Xue, Qi-Hua He, Xiao-Min Wang, and Ji-Sheng Han
Experimental Neurology 179, 28-37 (2003),-0001,():
-1年11月30日
It has been reported recently that the immunosuppressant FK506 produced neurotrophic and neuroprotective effects on dopaminergic neurons in vitro and in vivo. We investigated whether tripchlorolide, an immunosuppressive extract of Chinese herb Tripterygium wilfordii Hook F, could exert similar neurotrophic and neuroprotective effects similar to those of FK506. It was found that tripchlorolide promoted axonal elongation and protected dopaminergic neurons from a neurotoxic lesion induced by 1-methyl-4-phenylpyridinium ion (MPP+) at concentrations of as low as 10-12 to 10-8 M. In situ hybridization study revealed that tripchlorolide stimulated brain-derived neurotrophic factor (BDNF) mRNA expression. In vivo administration of tripchlorolide (1ug/kg, ip) for 28 days effectively attenuated the rotational behavior challenged by D-amphetamine in the model rats by transection of the medial forebrain bundle. In addition, tripchlorolide treatment (0.5 or 1ug/kg/day for 28 days) increased the survival of dopaminergic neurons in substantia nigra pars compacta by 50 and 67%, respectively. Moreover, tripchlorolide markedly prevented the decrease in amount of dopamine in the striatum of model rats. Taken together, our data provide the first evidence that tripchlorolide acts as a neuroprotective molecule that rescues MPP+ or axotomy-induced degeneration of dopaminergic neurons, which may imply its therapeutic potential for Parkinson’s disease. The underlying mechanism may be relevant to its neurotrophic effect and its efficacy in stimulating the expression of BDNF.
tripchlorolide, Tripterygium wilfordii Hook F, immunosuppressant, Chinese herb, neurotrophic, brain-derived neurotrophic factor, Parkinson', s disease.,
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王晓民, M. FANG, Y. WANG, Q. H. HE, Y. X. SUN, L. B. DENG, X. M. WANG AND J. S. HAN*
M. Fang et al./Neuroscience 504 117(2003)503-512,-0001,():
-1年11月30日
Neurotrophic factors, such as nerve growth factorand brain-derived neurotrophic factor, are members of thestructurally related neurotrophin family that play importantroles in pain modulation. Although there are also indicationsfor the involvement of glial cell line-derived neurotrophicfactor (GDNF), it is unclear whether and how GDNF is involvedin inflammatory pain. In the present study, we studiedthe expression pattern of GDNF in dorsal root ganglia (DRG)and spinal cord, using confocal microscopy. We demonstratethat GDNF is well associated with nonpeptidergic pain pathwayand that GDNF could possibly be anterogradely transportedfrom DRG neurons to superficial spinal cord dorsalhorn. We also studied the dynamic changes of GDNF expressionin rats during chronic inflammation using injection ofcomplete Freund's adjuvant as a model of chronic pain. Wefound that GDNF was down-regulated in both dorsal rootganglia and spinal cords 2 weeks after arthritis induction. Toassess the impact of this down-regulation on pain transmission,we used a function-blocking antibody against GDNFdelivered intrathecally in the same chronic-pain animal models.Injection of this antibody to GDNF produced no immediateeffect, but decreased the delayed, bilateral hyperalgesiainduced from a unilateral injection of complete Freund’s adjuvant.The effect of this antibody coincided with the downregulationof GDNF immunoreactivity in response to inflammation,suggesting that GDNF supports biochemicalchanges that contribute to hyperalgesia. © 2003 IBRO. Publishedby Elsevier Science Ltd. All rights reserved.
GDNF,, pain pathway,, nociception,, arthritis,, IB4.,
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