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研究领域

1、在神经退行性疾病体内外模型中研究天然药物中活性成分对神经元凋亡通路的调节作用.  神经元选择性凋亡是多种神经退行性疾病等的显著特征。我们的主要研究方向是在阿尔茨海默氏病 (Alzheimer' s Disease, AD)、帕金森氏病(Parkinson' s Disease, PD)和脑缺血(Ischemia)等多种细胞和动物模型上研究天然药物中活性成分对神经元凋亡信号转到通路的的作用机制。 2、天然药物中活性成分对胶质细胞的作用机制  近年来,越来越多的证据表明,胶质细胞在神经退行性疾病发生、发展过程中可能起重要作用。胶质细胞激活后释放的多种物质对神经元凋亡和调节突触传递等各种神经活动起重要调控作用。我们的研究以神经系统的胶质细胞为研究重点,从细胞、分子以及膜受体水平探讨天然药物中活性成分的调节作用 3、天然药物中活性成分在神经元膜受体和离子通道上的靶向作用  神经元膜上的受体和离子通道对于控制神经元的兴奋性、调节突触功能以及神经元内各种离子的动态平衡至关重要,而且膜受体和离子通道与神经退行性疾病的脑部病理性改变密切相关。我们利用基因工程和电生理技术,研究天然药物中活性成分在神经保护中的新途径。 利用形态学﹑遗传学﹑电生理学﹑分子生物学﹑生物化学和行为学等多学科的综合技术手段,研究天然中草药中神经活性成分对神经退行性疾病的细胞与分子作用机制

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Bo Jiang*, Jing Du, Jian-hui Liu, Yong-Ming Bao and Li-Jia Catalpol attenuates the neurotoxicity induced by β-Amyloid1-42 in cortical neuron-glia cultures. Brain research 2008, 1188(10):139-147 Liu YM, Jiang B*, An LJ, Bao YM. Protocatechuic acid inhibits apoptosis by mitochondrial dysfunction in rotenone-induced PC12 cells. Toxicology in Vitro. 2008, 22, 430-437 Tian YY, An LJ, Duan YL, Chen J, Jiang B*. Catalpol protects dopaminergic neurons from LPS-induced neurotoxicity in mesencephalic neuron-glia cultures. life science 2006,80: 193–199 Xiu Li Zhang, Bo Jiang, Zhi Bo Li, Shuang Hao, Li Jia An. Catalpol ameliorates cognition deficits and attenuates oxidative damage in the brain of senescent mice induced by D-galactose.. Pharmacology, Biochemistry and Behavior 2007, 88: 64–72 Tian YY, Jiang B*, An LJ, Bao YM. Neuroprotective effect of catalpol against MPP+-induced oxidative stress in mesencephalic neurons. European Journal of Pharmacology 2007,568: 142–148  Mao YR, Jiang L, Duan YL, Jiang B*, An LJ. Efficacy of catalpol as protectant against oxidative stress and mitochondrial dysfunction on rotenone-induced toxicity in mice brain. Environmental Toxicology and Pharmacology 2007, 23: 314-318 Jiang B, Liu JH, Bao YM, An LJ*. Catalpol inhibits apoptosis in hydrogen peroxide-induced PC12 cells by preventing cytochrome c release and inactivating of caspase cascade. Toxicon 2004, 43: 53-59 Jiang B*, Bao YM, Li ZG, Cheng L, An LJ. Protection by puerarin against MPP+-induced neurotoxicity in PC12 cells mediated by inhibiting mitochondrial dysfunction and caspase-3-like activation. Neurosci Res. 2005, 53(2):183-188 Jiang L, Jiang B*, Wang Z, Wang Y, Liu J. In situ prepared Al-Si alloy matrix composites reinforced by γ-Al2O3. J. Univ. Sci.Technol. Beijing 2007,14(6):1-5 Guan S, Jiang B, Bao YM, An LJ. Protocatechuic acid suppresses MPP+-induced mitochondrial dysfunction and apoptotic cell death in PC12 cells. Food and Chemical Toxicology 2006, 44(10):1659-1666

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