Xi Can Tang

Chinese Academy of Sciences, Peping, Beijing, China

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Publications (45)127.08 Total impact

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    ABSTRACT: Considerable studies indicate huperzine A is a promising natural product to suppress neuronal damages induced by β-amyloid (Aβ), a key pathogenic event in the Alzheimer's disease (AD). As an extension, the present study for the first time explored whether the beneficial profiles of huperzine A against oligomeric Aβ(42) induced neurotoxicity are associated with the accumulation and detrimental function of intraneuronal/mitochondrial Aβ, on the basis of the emerging evidence that intracellular Aβ is more relevant to AD progression as compared with extracellular Aβ. Huperzine A treatment was shown to significantly attenuate the neurotoxicity of oligomeric Aβ(42), as demonstrated by increased neuronal viability. Interestingly, our results proved that exogenous Aβ(42) could accumulate intraneuronally in a dose- and time-dependent manner, while huperzine A treatment markedly reduced the level of intracellular Aβ(42). Moreover, huperzine A treatment rescued mitochondrial dysfunction induced by oligomeric Aβ(42), including adenosine triphosphate (ATP) reduction, reactive oxygen species (ROS) overproduction and membrane potential depolarization. Further study demonstrated that huperzine A also significantly reduced the level of Aβ(42) in the mitochondria-enriched subcellular fractions, as well as the Aβ(42) fluorescent signals colocalized with mitochondrial marker. This study indicates that interfering intracellular Aβ especially mitochondrial Aβ accumulation, together with ameliorating Aβ-associated mitochondrial dysfunction, may contribute to the protective effects of huperzine A against Aβ neurotoxicity. Above results may shed more light on the pharmacological mechanisms of huperzine A and provide important clues for discovering novel therapeutic strategies for AD.
    PLoS ONE 05/2015; 10(5):e0128366. DOI:10.1371/journal.pone.0128366 · 3.23 Impact Factor
  • Chun Yan Ye · Yun Lei · Xi Can Tang · Hai Yan Zhang ·
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    ABSTRACT: The main purpose of the present study is to investigate the influence of donepezil, a well-known acetylcholinesterase (AChE) inhibitor, on amyloid-β (Aβ)-associated mitochondrial dysfunction, in order to gain a better understanding of the neuroprotective effects of this clinically used anti-Alzheimer's disease (AD) drug. First, our study verifies the ameliorative effects of donepezil on behavioral deficits in both working memory and anxiety in APP/PS1 double transgenic mice, at a time point that AChE is not inhibited. Meanwhile, we demonstrate that donepezil enhances the resistance of brain mitochondria of APP/PS1 mice to the induction of mitochondrial permeability transition (MPT) by calcium ions. Moreover, the level of mitochondrial Aβ in the brain of donepezil-treated APP/PS1 transgenic mice is significantly lower than that of vehicle-treated APP/PS1 mice. Our in vitro study using isolated mitochondria from rat brains, which is expected as an AChE-free subcellular system, further confirms the ameliorative effects of donepezil on oligomeric Aβ1-42 induced mitochondrial swelling and ATP reduction. In addition, donepezil treatment also significantly blocks the Aβ accumulation in the isolated mitochondria. Our study reported for the first time that the protective effects of donepezil against Aβ-associated mitochondrial dysfunction are closely associated with the reduction of Aβ accumulation in the mitochondria. Above observation led us to assume that, besides potent AChE inhibitory effects, other non-cholinergic mechanisms may be involved in the neuroprotective profiles of donepezil. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Neuropharmacology 03/2015; 95. DOI:10.1016/j.neuropharm.2015.02.020 · 5.11 Impact Factor
  • Zhi Ruan · Hong Min Wang · Xi Can Tang · Wei Min Zhao · Hai Yan Zhang ·

    Neurobiology of Aging 03/2014; 35:S27. DOI:10.1016/j.neurobiolaging.2014.01.132 · 5.01 Impact Factor
  • Xu Jie Wang · Luo Yi Wang · Yan Fu · Jian Wu · Xi Can Tang · Wei Min Zhao · Hai Yan Zhang ·
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    ABSTRACT: Oxidative stress plays an important role in the pathological processes of various neurodegenerative diseases. In this study, we investigated the neuroprotective effects of (M)-bicelaphanol A, which has been the first dimeric podocarpane type trinorditerpene isolated from Celastrus orbiculatus, against hydrogen peroxide (H2O2)-induced injury in human SH-SY5Y neuroblastoma cells. Our study showed that cells pretreated with (M)-bicelaphanol A significantly attenuated H2O2-induced cell viability reduction and cell apoptosis. These neuroprotective effects of (M)-bicelaphanol A were associated with a reduction of reactive oxygen species and an increase in the level of adenosine triphosphate. In addition, (M)-bicelaphanol A pretreatment markedly increased the phosphorylation level of Akt in SH-SY5Y cells. In conclusion, our results for the first time demonstrate that the protection of (M)-bicelaphanol A on SH-SY5Y cells against H2O2-induced oxidative stress may attribute, at least partially, to its attenuation of mitochondrial dysfunction and activation of Akt signaling pathway. Above results shed more light on the molecular mechanisms involved in the neuroprotective effects of (M)-bicelaphanol A, which could be a potential drug candidate for the treatment of oxidative stress-associated neurodegenerative diseases.
    Phytomedicine: international journal of phytotherapy and phytopharmacology 06/2013; 20(12). DOI:10.1016/j.phymed.2013.04.017 · 3.13 Impact Factor
  • Bing Zhang · Xi Can Tang · Hai Yan Zhang ·
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    ABSTRACT: Although many post-mortem studies have found evidence of central insulin resistance in Alzheimer's disease (AD) patients, results on changes of central insulin-like growth factor-1 (IGF-1) signaling in the pathological process of AD remain controversial. In the present study, we observed the activation states of IGF-1 downstream signaling in brain slices of transgenic mice carrying APPswe/PS1dE9 mutations (APP/PS1 mice) at both early and late stages (ex vivo) and further investigated the involvement of oligomeric β-amyloid (Aβ) and Aβ-enriched culture medium (CM) on IGF-1 sensitivity employing neuronal models (in vitro). In 6- and 18-month-old APP/PS1 mice, the phosphorylations of IGF-1 receptor (IGF-1R) and Akt in response to IGF-1 stimulation were significantly reduced in the hippocampal and cortical slices, whereas IGF-1R protein expression and mRNA levels of IGF-1 and IGF-1R in the hippocampal slices were significantly higher than that in wild-type mice. In agreement with these results, reduced IGF-1 sensitivity was verified in APP and PS1 double stably transfected CHO cells; moreover, IGF-1 stimulated phosphorylations of IGF-1R and Akt were also markedly weakened by oligomeric Aβ or Aβ-enriched CM posttreatment in CHO cells without APP/PS1-transfected (K1 cells) and primary hippocampal neurons. These observations indicate that the impaired central IGF-1 sensitivity at early and late stages of APP/PS1 transgenic mice might be attributable, at least partially, to the overproduced Aβ, especially the oligomeric Aβ. These findings may shed new light on the mechanisms underlying the defective IGF-1 signaling in AD pathogenesis and provide important clues for AD drug discovery. © 2013 Wiley Periodicals, Inc.
    Journal of Neuroscience Research 05/2013; 91(5). DOI:10.1002/jnr.23201 · 2.59 Impact Factor
  • Xin Gao · Chun Yan Zheng · Guo Wei Qin · Xi Can Tang · Hai Yan Zhang ·
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    ABSTRACT: Accumulating evidence suggests that β-amyloid (Aβ)-induced oxidative DNA damage and mitochondrial dysfunction may initiate and contribute to the progression of Alzheimer's disease (AD). This study evaluated the neuroprotective effects of S-52, a novel nootropic compound, on Aβ-induced mitochondrial failure. In an established paradigm of moderate cellular injury induced by Aβ, S-52 was observed to attenuate the toxicity of Aβ to energy metabolism, mitochondrial membrane structure, and key enzymes in the electron transport chain and tricarboxylic acid cycle. In addition, S-52 also effectively inhibited reactive oxygen species accumulation dose dependently not only in Aβ-harmed cells but also in unharmed, normal cells. The role of S-52 as a scavenger of free radicals is involved in the antioxidative effect of this compound. The beneficial effects on mitochondria and oxidative stress extend the neuroprotective effects of S-52. The present study provides crucial information for better understanding the beneficial profiles of this compound and discovering novel potential drug candidates for AD therapy.
    Journal of Neuroscience Research 10/2012; 90(10):1981-8. DOI:10.1002/jnr.23086 · 2.59 Impact Factor
  • Ying Wang · Xi Can Tang · Hai Yan Zhang ·
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    ABSTRACT: Huperzine A (HupA) is a potent acetylcholinesterase inhibitor (AChEI) used in the treatment of Alzheimer's disease (AD). Recently, HupA was shown to be active in modulating the nonamyloidogenic metabolism of β-amyloid precursor protein (APP) in APP-transfected human embryonic kidney cell line (HEK293swe). However, in vivo research concerning the mechanism of HupA in APP transgenic mice has not yet been fully elucidated. The present study indicates that the loss of dendritic spine density and synaptotagmin levels in the brain of APPswe/presenilin-1 (PS1) transgenic mice was significantly ameliorated by chronic HupA treatment and provides evidence that this neuroprotection was associated with reduced amyloid plaque burden and oligomeric β-amyloid (Aβ) levels in the cortex and hippocampus of APPswe/PS1dE9 transgenic mice. Our findings further demonstrate that the amelioration effect of HupA on Aβ deposits may be mediated, at least in part, by regulation of the compromised expression of a disintegrin and metalloprotease 10 (ADAM10) and excessive membrane trafficking of β-site APP cleavage enzyme 1 (BACE1) in these transgenic mice. In addition, extracellular signal-regulated kinases 1/2 (Erk1/2) phosphorylation may also be partially involved in the effect of HupA on APP processing. In conclusion, our work for the first time demonstrates the neuroprotective effect of HupA on synaptic deficits in APPswe/PS1dE9 transgenic mice and further clarifies the potential pharmacological targets for this protective effect, in which modulation of nonamyloidogenic and amyloidogenic APP processing pathways may be both involved. These findings may provide adequate evidence for the clinical and experimental benefits gained from HupA treatment.
    Journal of Neuroscience Research 02/2012; 90(2):508-17. DOI:10.1002/jnr.22775 · 2.59 Impact Factor
  • Juan Wang · Hai Yan Zhang · Xi Can Tang ·
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    ABSTRACT: Chronic cerebral hypoperfusion has been suggested to contribute to the progression of dementia. Inflammation and white matter lesion (WML) are involved in the pathologic process. This study investigated whether huperzine A, a natural acetylcholinesterase (AChE) inhibitor, has beneficial effects on long-lasting inflammation as well as cognitive impairment in a rat model of cerebral hypoperfusion and how it plays these roles. Chronic cerebral hypoperfusion was induced by occlusion of bilateral common carotid arteries (two-vessel occlusion; 2VO). Huperzine A was initially given 150 min after 2VO and daily for 3, 7, 14, and 28 days. Learning and memory dysfunction as tested by Morris water maze performance was observed in 2VO-operated rats and was significantly improved by huperzine A treatment. WML and activation staining of immune cells were evaluated by Klüver-Barrera (KB) and immunohistochemistry, respectively. Myelin damage and increased immunostains were found in optic tract at all indicated days. Huperzine A treatment significantly ameliorated all these phenomena. Moreover, huperzine A also suppressed overexpression of the inflammatory factor tumor necrosis factor-alpha (TNF-alpha) and overphosphorylation of JNK and p38 mitogen-activated protein kinases (MAPKs) in a cell model of chronic hypoxia. Preincubation with mecamylamine (MEC), a nicotinic acetylcholine receptor (nAChR) antagonist, for 30 min before hypoxia notably reversed the effects of huperzine A on TNF-alpha production and MAPKs phosphorylation. In conclusion, delayed and chronic administration of huperzine A could protect against 2VO-induced cognitive impairment, which might be related to its beneficial effects on WML, and the nAChR-dependent cholinergic anti-inflammation pathway plays an important role.
    Journal of Neuroscience Research 11/2009; 88(4):807-15. DOI:10.1002/jnr.22237 · 2.59 Impact Factor
  • Xin Gao · Chun Yan Zheng · Ling Yang · Xi Can Tang · Hai Yan Zhang ·
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    ABSTRACT: Our previous work in cells and animals showed that mitochondria are involved in the neuroprotective effect of huperzine A (HupA). In this study, the effects of HupA on isolated rat brain mitochondria were investigated. In addition to inhibiting the Abeta(25-35) (40 microM)-induced decrease in mitochondrial respiration, adenosine 5'-triphosphate (ATP) synthesis, enzyme activity, and transmembrane potential, HupA (0.01 or 0.1 microM) effectively prevented Abeta-induced mitochondrial swelling, reactive oxygen species increase, and cytochrome c release. More interestingly, administration of HupA to isolated mitochondria promoted the rate of ATP production and blocked mitochondrial swelling caused by normal osmosis. These results indicate that HupA protects mitochondria against Abeta at least in part by preserving membrane integrity and improving energy metabolism. These direct effects on mitochondria further extend the noncholinergic functions of HupA.
    Free Radical Biology and Medicine 04/2009; 46(11):1454-62. DOI:10.1016/j.freeradbiomed.2009.02.028 · 5.74 Impact Factor
  • Chun Yan Zheng · Hai Yan Zhang · Xi Can Tang ·
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    ABSTRACT: Mitochondrial dysfunction has been proved to contribute to ischemia-induced brain damage. In this study, which used a rat middle cerebral artery occlusion (MCAO) model, the protective effects of huperzine A (HupA) against mitochondrial dysfunction and brain damage were investigated. MCAO for 45 min followed by 4 hr of reperfusion significantly impaired the activities of mitochondrial respiratory chain enzymes (complex I, complex II-III, and complex IV) and alpha-ketoglutarate dehydrogenase, increased the production of reactive oxygen species (ROS), and induced mitochondrial swelling. Pretreatment of HupA at 0.1 mg/kg significantly preserved respiratory chain enzyme activities, decreased ROS production, and attenuated mitochondrial swelling. It could also significantly attenuate the neurological deficits (after 4 or 24 hr reperfusion) and reduce infarct volumes (after 24 hr reperfusion). Moreover, HupA protected isolated nonsynaptosomal mitochondria from calcium-induced damage in vitro by preserving mitochondrial membrane potential and decreasing ROS production. Overall, the present study indicates that HupA can ameliorate MCAO-induced mitochondrial dysfunction, and this might partially contribute to its protective effect on brain damage after 24 hr of reperfusion.
    Journal of Neuroscience Research 08/2008; 86(11):2432-40. DOI:10.1002/jnr.21681 · 2.59 Impact Factor
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    ABSTRACT: Huperzine A (HupA), a novel Lycopodium alkaloid isolated from Chinese folk medicine Huperzia serrata (Qian Ceng Ta), is a potent, selective and well-tolerated inhibitor of acetylcholinesterase (AChE). It has been proven to significantly improve the learning and memory impairment in Alzheimer's disease (AD) and vascular dementia (VaD) patients in China. Interestingly, our recent data indicate that HupA also possesses other protective functions. This paper will give an overview on the protective effects of HupA, which includes regulating beta-amyloid precursor protein (APP) metabolism, protecting against Abeta-mediated oxidative stress, apoptosis and mitochondrial dysfunction, as well as anti-inflammation. The multiple neuroprotective effects of HupA might yield additional beneficial effects in AD and VaD therapy.
    Chemico-Biological Interactions 06/2008; 175(1-3):396-402. DOI:10.1016/j.cbi.2008.04.049 · 2.58 Impact Factor
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    Zhi Fei Wang · Jin Yan · Yan Fu · Xi Can Tang · Song Feng · Xu Chang He · Dong Lu Bai ·
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    ABSTRACT: (1) This study was to evaluate the anti-cholinesterase (ChE), cognition enhancing and neuroprotective effects of FS-0311, a bis-huperzine B derivative. (2) ChE activity was evaluated using a spectrophotometric method. Cognitive deficits in mice were induced by scopolamine or transient brain ischemia and reperfusion. Water maze was used to detect the cognitive performance. PC12 cell injury was induced by beta-amyloid 25-35 (Abeta(25-35)), oxygen-glucose deprivation (OGD), or staurosporine treatment. (3) FS-0311 was a potent, highly specific inhibitor of acetylcholinesterase (AChE). FS-0311 bound to AChE in a reversible manner, causing linear mixed-type inhibition. FS-0311 had a high oral bioavailability and a long duration of AChE inhibitory action in vivo. FS-0311 was found to antagonize cognitive deficits induced by scopolamine or transient brain ischemia and reperfusion in a water maze task. FS-0311 possessed the ability to protect PC12 cells against Abeta(25-35) peptide toxicity, OGD insult and staurosporine-induced apoptosis. The neuroprotective effects of FS-0311 appeared to reflect an attenuation of oxidative stress. (4) With the profile of anti-ChE and neuroprotective activities, FS-0311 might be a promising candidate in neurodegenerative diseases, such as Alzheimer's disease and Vascular dementia.
    Cellular and Molecular Neurobiology 03/2008; 28(2):245-61. DOI:10.1007/s10571-007-9199-0 · 2.51 Impact Factor
  • Hai Yan Zhang · Han Yan · Xi Can Tang ·
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    ABSTRACT: The use of acetylcholinesterase inhibitors to decrease the breakdown of the neurotransmitter acetylcholine has been the main symptomatic therapy for mild to moderate Alzheimer's patients, though the etiology of Alzheimer's disease remains unclear and seems to involve multiple factors. Further evidence has indicated that some of these acetylcholinesterase inhibitors also have non-cholinergic functions on the pathogenesis of Alzheimer's disease including the formation and deposition of beta-amyloid. Huperzine A, a potent and reversible inhibitor of acetylcholinesterase that was initially isolated from a Chinese herb, has been found to improve cognitive deficits in a broad range of animal models and has been used for Alzheimer's disease treatment in China. The novel neuroprotective effects of huperzine A might yield beneficial effects in Alzheimer's disease therapy and provide a potential template for the design of new selective and powerful anti-Alzheimer's drugs. The present paper gives an overview on the neuroprotective effects of huperzine A beyond its acetylcholinesterase inhibition. These effects include regulating beta-amyloid precursor protein metabolism, protecting against beta-amyloid-mediated oxidative stress and apoptosis. The structure-function relationship of huperzine A is also discussed.
    Cellular and Molecular Neurobiology 03/2008; 28(2):173-83. DOI:10.1007/s10571-007-9163-z · 2.51 Impact Factor
  • Yan Qi Liang · Xiao Tian Huang · Xi Can Tang ·
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    ABSTRACT: (1) Huperzine A, a promising therapeutic agent for Alzheimer's disease (AD), was tested for its effects on cholinergic and monoaminergic dysfunction induced by injecting beta-amyloid peptide-(1-40) into nucleus basalis magnocellularis of the rat. (2) Bilateral injection of 10 microg beta-amyloid peptide-(1-40) into nucleus basalis magnocellularis produced local deposits of amyloid plaque and functional abnormalities detected by microdialysis. In medial prefrontal cortex, reductions in the basal levels and stimulated release of acetylcholine, dopamine, norepinephrine, and 5-hydroxytryptamine were observed. However, oral huperzine A (0.18 mg/kg, once daily for 21 consecutive days) markedly reduced morphologic abnormalities at the injection site in rats infused with beta-amyloid peptide-(1-40). Likewise, this treatment ameliorated the beta-amyloid peptide-(1-40)-induced deficits in extracellular acetylcholine, dopamine, and norepinephrine (though not 5-hydroxytryptamine) in medial prefrontal cortex, and lessened the reduction in nicotine or methoctramine-stimulated release of acetylcholine and K(+)-evoked releases of acetylcholine and dopamine. (3) The present results provide the first direct evidence that huperzine A acts to oppose neurotoxic effects of beta-amyloid peptide on cholinergic, dopaminergic, and noradrenergic systems of the rat forebrain.
    Cellular and Molecular Neurobiology 02/2008; 28(1):87-101. DOI:10.1007/s10571-007-9158-9 · 2.51 Impact Factor
  • Hai Yan Zhang · Xi Can Tang ·
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    ABSTRACT: China is well known for its long history of traditional Chinese medicine (TCM), which has endured for thousands of years. The use of TCM requires complex recipes and formulae derived from historical and anecdotal evidence of Chinese medicinal practitioners. Although western drugs were brought into China over a hundred years ago, TCM is still widely used in China based on its unique theory and reliable clinical effects. Under the present conditions of economic globalization, a new wave of modernization of TCM is occurring along with a trend of exploring TCM as a source for the discovery of new therapeutic chemicals and drugs. Hence, a large number of active compounds have been isolated from Chinese herbal extracts and proved to possess prominent clinical effects in the treatment of various diseases including neurological disorders (Howes and Houghton 2003; Chen et al. 2007; Yan et al. 2007). Through persistent attempts and practices, and based on the accumulated experience in disease prevention, several herbal extracts have been found with remarkable effectiveness in the therapy of dementia including Alzheimer’s disease (AD) (Howes and Houghton 2003). Among them, huperzine A (HupA), a novel lycopodium alkaloid isolated from the Chinese medicinal herb Huperzia serrata (Qian Ceng Ta), has been found to improve cognitive deficits in a broad range of animal models and patients with AD and vascular dementia. This agent is currently in phase IV Clinical trial in China for AD therapy, and in clinical trials for the treatment of age-related memory deficiency in the United States. In addition, HupA could also improve the memory and cognitive deficits caused by other pathogenies, such as schizophrenia, brain trauma, and iodine deficiency. HupA is not only a reversible, potent, and selective acetylcholinesterase inhibitor, but also possesses multi-target neuroprotective effects
    Cellular and Molecular Neurobiology 02/2008; 28(1):9-12. DOI:10.1007/s10571-007-9239-9 · 2.51 Impact Factor
  • Han Yan · Hai Yan Zhang · Xi Can Tang ·
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    ABSTRACT: This study is to explore the involvement of muscarinic acetylcholine receptors/protein kinase C cascade and the mitogen-activated protein kinase pathway in the effect of huperzine A on the secretory amyloid precursor protein-alpha. Upregulation of secretory amyloid precursor protein-alpha by huperzine A was attenuated by muscarinic acetylcholine receptor antagonist (specifically by M1-muscarinic acetylcholine receptor antagonist), and markedly blocked (-37.7%) by protein kinase C inhibitor as well. Meanwhile, huperzine A can activate the phosphorylation of mitogen-activated protein kinase and, accordingly, partly restored PD98059-decreased secretory amyloid precursor protein-alpha secretion. In addition, huperzine A largely inhibited (-55.4%) acetylcholinesterase activity of the cell line. Our results suggest that activated M1-muscarinic acetylcholine receptor/protein kinase C pathway and mitogen-activated protein kinase signaling are involved in the process of huperzine A enhancing the secretory amyloid precursor protein-alpha secretion.
    Neuroreport 05/2007; 18(7):689-92. DOI:10.1097/WNR.0b013e3280c1e28c · 1.52 Impact Factor
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    Zhi Fei Wang · Xi Can Tang ·
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    ABSTRACT: The protective effects of huperzine A against oxygen-glucose deprivation (OGD)-induced injury in C6 cells were investigated. OGD for 6h and reoxygenation for 6h enhanced phosphorylation and degradation of IkappaBalpha and nuclear translocation of nuclear factor-kappa B (NF-kappaB), triggered overexpression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and nitric oxide (NO) in C6 cells. Along with inhibiting acetylcholinesterase activity, treatment with 1 microM huperzine A inhibited activation of NF-kappaB, attenuated iNOS, COX-2 and NO overexpression, and promoted survival in C6 cells subjected to OGD insult. The protective effects of huperzine A were partly mediated by "cholinergic anti-inflammatory pathway" through alpha7 nicotinic acetylcholine receptor.
    FEBS Letters 03/2007; 581(4):596-602. DOI:10.1016/j.febslet.2007.01.016 · 3.17 Impact Factor
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    Han Yan · Lin Li · Xi Can Tang ·
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    ABSTRACT: Senile dementia is a syndrome in the elderly involving deficits in memory and cognition. There has been a long history of research and medical practice in dementia in China, during which the ancient Chinese people have formed a whole theory and accumulated abundant experience in the treatment of dementia. During recent decades, with new theories and technologies being digested and integrated, progress has been made in the medical and pharmacy research on senile dementia in China. In this review, we will focus on the traditional opinion, clinical practice, and recent progress in pharmacological research in China towards the treatment of dementia. We also discuss the potential trends of global convergence.
    Clinical Interventions in Aging 02/2007; 2(2):201-8. · 2.08 Impact Factor
  • Hai Yan Zhang · Xi Can Tang ·
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    ABSTRACT: In recent years, the most common pharmacological treatment for Alzheimer's disease (AD) has been acetylcholinesterase (AChE) inhibition. However, this single-target approach has limited effectiveness and there is evidence that a multitarget approach might be more effective. Huperzine A (HupA), a novel alkaloid isolated from a Chinese herb, has neuroprotective effects that go beyond the inhibition of AChE. Recent data have demonstrated that HupA can ameliorate the learning and memory deficiency in animal models and AD patients. Its potentially beneficial actions include modification of beta-amyloid peptide processing, reduction of oxidative stress, neuronal protection against apoptosis, and regulation of the expression and secretion of nerve growth factor (NGF) and NGF signaling.
    Trends in Pharmacological Sciences 01/2007; 27(12):619-25. DOI:10.1016/j.tips.2006.10.004 · 11.54 Impact Factor
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    Xi Can Tang · Yi Fan Han ·
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    ABSTRACT: HupA, a novel alkaloid isolated from the Chinese medicinal herb Huperzia serrata, is a reversible, potent, and selective inhibitor of AChE. Compared with other well-known AChEIs, such as physostigmine, galanthamine, tacrine, and even donepezil, HupA has better penetration through the blood-brain barrier, higher oral bioavailability, and longer duration of AChE inhibitory action. HupA exhibited memory-enhancing efficacy in a broad range of animal models of cognitive impairment. Double-blind and placebo-controlled clinical trials have demonstrated that HupA produced significant improvements in memory deficiencies in aged patients and patients with AD. Furthermore, both animal and clinical safety testings showed that HupA was devoid of unexpected toxicity, particularly the dose-limiting hepatotoxicity induced by tacrine. These encouraging preclinical and clinical findings suggest that HupA is a highly promising candidate for clinical development as a symptomatic treatment for AD and other memory disorders related to a central cholinergic deficiency.
    CNS Drug Reviews 06/2006; 5(3):281 - 300. DOI:10.1111/j.1527-3458.1999.tb00105.x · 4.92 Impact Factor

Publication Stats

2k Citations
127.08 Total Impact Points


  • 1995-2015
    • Chinese Academy of Sciences
      • State Key Laboratory of Drug Research
      Peping, Beijing, China
  • 2001-2008
    • Shanghai Institutes for Biological Sciences
      Shanghai, Shanghai Shi, China