The neuroprotective effects of Nokyongdaebo-tang(Lurongdabutang) treatment in pathological Alzheimer's disease model of neural tissues

Objectives : Alzheimer's disease(AD) is the most common form of dementia, which is characterized by progressive deterioration of memory and higher cortical functions that ultimately results in total degradation of intellectual and mental activities. Nokyongdaebo-tang(Lurongdabutang) has been usually used for the treatment for the deficiency syndrome dementia and amnesia. This experiment was designed to investigate the effect of the Nokyongdaebo-tang(Lurongdabutang) hot water extract on pathological AD model. Methods : The effects of the Nokyongdaebo-tang(Lurongdabutang) hot water extract on cultured spinal cord cells induced by -amyloid were investigated. The effects of the Nokyongdaebo-tan(Lurongdabutang) hot water extract on the memory deficit mice induced by scopolamine were investigated. Results : 1. -amyloid treatment on cultured spinal cord cells increased both GFAP-staining intensity of astrocytes and caspase 3 immunoreactivity on cultured cells. Then, Nokyongdaebo-tang(Lurongdabutang) treatment reduced the labeling intensity for both GFAP and caspase 3 proteins in culture cells. 2. Scopolamine treatment into mice increased levels of GFAP-positive astrocytes and caspase 3-labeled cells of the hippocampal subfields dentate hilar region, CA3 and CA1 area. In vivo administration of Nokyongdaebo-tang(Lurongdabutang) attenuated labeling intensity for those two proteins in the same hippocampal areas. Similar effects were observed by the treatment of galanthamine, an inhibitor of acetylcholinesterase. Conclusions : This experiment shows that the Nokyongdaebo-tang(Lurongdabutang) may play a protective role in damaged neural tissues. Since neuronal damage seen in degenerative brains such as AD are largely unknown, the current data may provide possible insight into therapeutic strategies for AD treatments. Nokyongdaebo-tang(Lurongdabutang) might be effective for the prevention and treatment of AD.

[1]  D. Selkoe Alzheimer's disease. , 2011, Cold Spring Harbor perspectives in biology.

[2]  G. Hu,et al.  Pathological and biochemical alterations of astrocytes in ovariectomized rats injected with d-galactose: A potential contribution to Alzheimer's disease processes , 2008, Experimental Neurology.

[3]  Deborah L. Downey Pharmacologic management of Alzheimer disease. , 2008, The Journal of neuroscience nursing : journal of the American Association of Neuroscience Nurses.

[4]  P. Mcgeer,et al.  Inflammatory aspects of Alzheimer disease and other neurodegenerative disorders. , 2008, Journal of Alzheimer's disease : JAD.

[5]  Nicola Vanacore,et al.  Cholinesterase Inhibitors in Mild Cognitive Impairment: A Systematic Review of Randomised Trials , 2007, PLoS medicine.

[6]  R. Vassar Caspase-3 Cleavage of GGA3 Stabilizes BACE: Implications for Alzheimer's Disease , 2007, Neuron.

[7]  L. Saksida,et al.  Paradoxical Facilitation of Object Recognition Memory after Infusion of Scopolamine into Perirhinal Cortex: Implications for Cholinergic System Function , 2006, The Journal of Neuroscience.

[8]  M. Giovannini,et al.  Cholinergic dysfunction, neuronal damage and axonal loss in TgCRND8 mice , 2006, Neurobiology of Disease.

[9]  Zhigang He,et al.  Glial inhibition of CNS axon regeneration , 2006, Nature Reviews Neuroscience.

[10]  J. Standridge Vicious cycles within the neuropathophysiologic mechanisms of Alzheimer's disease. , 2006, Current Alzheimer research.

[11]  Maria do Carmo Carreiras,et al.  Galanthamine, a natural product for the treatment of Alzheimer's disease. , 2006, Recent patents on CNS drug discovery.

[12]  J. Dodart,et al.  Overview on Rodent Models of Alzheimer's Disease , 2005, Current protocols in neuroscience.

[13]  Y. Koshino,et al.  Correlation between astrocyte apoptosis and Alzheimer changes in gray matter lesions in Alzheimer's disease. , 2005, Journal of Alzheimer's disease : JAD.

[14]  M. Carreiras,et al.  Recent approaches to novel anti-Alzheimer therapy. , 2004, Current pharmaceutical design.

[15]  K. Hensley,et al.  Oxidative stress and neuroinflammation in Alzheimer's disease and amyotrophic lateral sclerosis: common links and potential therapeutic targets. , 2004, Journal of Alzheimer's disease : JAD.

[16]  Anne Eckert,et al.  Increased Apoptotic Cell Death in Sporadic and Genetic Alzheimer's Disease , 2003, Annals of the New York Academy of Sciences.

[17]  Friedrich Srienc,et al.  Automated flow cytometry for acquisition of time‐dependent population data , 2003, Cytometry. Part A : the journal of the International Society for Analytical Cytology.

[18]  R. Fields,et al.  New insights into neuron-glia communication. , 2002, Science.

[19]  J. Unger Glial reaction in aging and Alzheimer's disease , 1998, Microscopy research and technique.

[20]  G. Šimić,et al.  Volume and number of neurons of the human hippocampal formation in normal aging and Alzheimer's disease , 1997, The Journal of comparative neurology.

[21]  D. Borchelt,et al.  Age-related CNS disorder and early death in transgenic FVB/N mice overexpressing Alzheimer amyloid precursor proteins , 1995, Neuron.

[22]  L. Mucke,et al.  Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein , 1995, Nature.

[23]  A. Sirigu,et al.  What can preservation of autobiographic memory after muscarinic blockade tell us about the scopolamine model of dementia? , 1995, Neurology.

[24]  P. Greengard,et al.  The nature and metabolism of potentially amyloidogenic carboxyl-terminal fragments of the Alzheimer βA4-amyloid precursor protein: Some technical notes , 1992, Neurobiology of Aging.

[25]  K. Murakami,et al.  Formation of β-amyloid protein deposits in brains of transgenic mice , 1991, Nature.

[26]  M. Landon,et al.  Amyloid in Alzheimer's disease. , 1989, Biochemical Society transactions.