CLC number: R285.5
On-line Access: 2024-08-27
Received: 2023-10-17
Revision Accepted: 2024-05-08
Crosschecked: 2015-06-16
Cited: 1
Clicked: 4611
Jian-xiang Liu, Min-ying Zhu, Ci-yuan Feng, Hai-bin Ding, Ying Zhan, Zhan Zhao, Yue-min Ding. Bamboo leaf extract improves spatial learning ability in a rat model with senile dementia[J]. Journal of Zhejiang University Science B, 2015, 16(7): 593-601.
@article{title="Bamboo leaf extract improves spatial learning ability in a rat model with senile dementia",
author="Jian-xiang Liu, Min-ying Zhu, Ci-yuan Feng, Hai-bin Ding, Ying Zhan, Zhan Zhao, Yue-min Ding",
journal="Journal of Zhejiang University Science B",
volume="16",
number="7",
pages="593-601",
year="2015",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B1400249"
}
%0 Journal Article
%T Bamboo leaf extract improves spatial learning ability in a rat model with senile dementia
%A Jian-xiang Liu
%A Min-ying Zhu
%A Ci-yuan Feng
%A Hai-bin Ding
%A Ying Zhan
%A Zhan Zhao
%A Yue-min Ding
%J Journal of Zhejiang University SCIENCE B
%V 16
%N 7
%P 593-601
%@ 1673-1581
%D 2015
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1400249
TY - JOUR
T1 - Bamboo leaf extract improves spatial learning ability in a rat model with senile dementia
A1 - Jian-xiang Liu
A1 - Min-ying Zhu
A1 - Ci-yuan Feng
A1 - Hai-bin Ding
A1 - Ying Zhan
A1 - Zhan Zhao
A1 - Yue-min Ding
J0 - Journal of Zhejiang University Science B
VL - 16
IS - 7
SP - 593
EP - 601
%@ 1673-1581
Y1 - 2015
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1400249
Abstract: Senile dementia (SD) is a syndrome characterized by progressive neurological deterioration. Treatment for the disease is still under investigation. bamboo leaf extract (B-extract) has been known for its biological efficacy in anti-oxidant and anti-cancer activities. However, study on B-extract for its protection against dementia is very limited. The effect of B-extract on a rat model with SD was examined. B-extract improved spatial learning ability of the dementia rats. The hippocampus of dementia model rats showed reduced levels of acetylcholine (ACh), epinephrine (E), norepinephrine (NE), and dopamine (DA), and increased activities of acetylcholine esterase (AChE) and monoamine oxidase (MAO). Treatment with B-extract 20 mg/(kg·d) for 7 weeks significantly inhibited the enzyme activity compared with untreated dementia rats, and raised the levels of ACh, E, and DA in the hippocampus. In addition, treatment with B-extract elevated the level of γ-aminobutyric acid (GABA), but reduced the level of glutamate (Glu) in the brain. These data suggest that B-extract might be a potential drug in treating impairment of spatial memory in dementia rats by regulating the central neurotransmitter function.
[1]Alper, G., Girgin, F.K., Ozgonul, M., et al., 1999. MAO inhibitors and oxidant stress in aging brain tissue. Eur. Neuropsychopharmacol., 9(3):247-252.
[2]Alvarez, A., Opazo, C., Alarcon, R., et al., 1997. Acetylcholinesterase promotes the aggregation of amyloid-β-peptide fragments by forming a complex with the growing fibrils. J. Mol. Biol., 272(3):348-361.
[3]Checler, F., Turner, A.J., 2012. Journal of neurochemistry special issue on Alzheimer’s disease: ‘amyloid cascade hypothesis—20 years on’. J. Neurochem., 120(Suppl. 1):iii-iv.
[4]Choi, S., Park, M.S., Lee, Y.R., et al., 2013. A standardized bamboo leaf extract inhibits monocyte adhesion to endothelial cells by modulating vascular cell adhesion protein-1. Nutr. Res. Pract., 7(1):9-14.
[5]Chun, W., Johnson, G.V., 2007. The role of tau phosphorylation and cleavage in neuronal cell death. Front. Biosci., 12(1):733-756.
[6]Cui, X., Zuo, P., Zhang, Q., et al., 2006. Chronic systemic
[7]Deguil, J., Ravasi, L., Auffret, A., et al., 2013. Evaluation of symptomatic drug effects in Alzheimer’s disease: strategies for prediction of efficacy in humans. Drug Discov. Today Technol., 10(3):e329-e342.
[8]de Souza Silva, M.A., Lenz, B., Rotter, A., et al., 2013. Neurokinin3 receptor as a target to predict and improve learning and memory in the aged organism. PNAS, 110(37):15097-15102.
[9]Erickson, C.A., Barnes, C.A., 2003. The neurobiology of memory changes in normal aging. Exp. Gerontol., 38(1-2):61-69.
[10]Ferri, C.P., Prince, M., Brayne, C., et al., 2005. Global prevalence of dementia: a delphi consensus study. Lancet, 366(9503):2112-2117.
[11]Golde, T.E., Schneider, L.S., Koo, E.H., 2011. Anti-Aβ therapeutics in Alzheimer’s disease: the need for a paradigm shift. Neuron, 69(2):203-213.
[12]Gupta, V.K., Scheunemann, L., Eisenberg, T., et al., 2013. Restoring polyamines protects from age-induced memory impairment in an autophagy-dependent manner. Nat. Neurosci., 16(10):1453-1460.
[13]Hardy, J., 2006. Alzheimer’s disease: the amyloid cascade hypothesis: an update and reappraisal. J. Alzheimers Dis., 9(Suppl. 3):151-153.
[14]Ho, S.C., Liu, J.H., Wu, R.Y., 2003. Establishment of the mimetic aging effect in mice caused by
[15]Hoyert, D.L., Xu, J., 2012. Deaths: preliminary data for 2011. Natl. Vital. Stat. Rep., 61(6):1-51.
[16]Hureau, C., Sasaki, I., Gras, E., et al., 2010. Two functions, one molecule: a metal-binding and a targeting moiety to combat Alzheimer’s disease. ChemBioChem, 11(7):950-953.
[17]Iqbal, K., Alonso Adel, C., Chen, S., et al., 2005. Tau pathology in Alzheimer disease and other tauopathies. Biochim. Biophys. Acta, 1739(2-3):198-210.
[18]Lamberty, Y., Gower, A.J., Gobert, J., et al., 1992. Behavioural, biochemical and histological effects of AF64A following injection into the third ventricle of the mouse. Behav. Brain Res., 51(2):165-177.
[19]Lee, M.J., Park, W.H., Song, Y.S., et al., 2008. Effect of bamboo culm extract on oxidative stress and genetic expression: bamboo culm extract ameliorates cell adhesion molecule expression and NFκB activity through the suppression of the oxidative stress. Clin. Nutr., 27(5):755-763.
[20]Lewczuk, P., Esselmann, H., Bibl, M., et al., 2004. Tau protein phosphorylated at threonine 181 in CSF as a neurochemical biomarker in Alzheimer’s disease: original data and review of the literature. J. Mol. Neurosci., 23(1-2):115-122.
[21]Liu, L.T., Xu, Y., Tang, P., 2010. Mechanistic insights into xenon inhibition of NMDA receptors from MD simulations. J. Phys. Chem. B, 114(27):9010-9016.
[22]Lopes, J.P., Oliveira, C.R., Agostinho, P., 2010. Neurodegeneration in an Aβ-induced model of Alzheimer’s disease: the role of Cdk5. Aging Cell, 9(1):64-77.
[23]Mandel, S., Amit, T., Bar-Am, O., et al., 2007. Iron dysregulation in Alzheimer’s disease: multimodal brain permeable iron chelating drugs, possessing neuroprotective-neurorescue and amyloid precursor protein-processing regulatory activities as therapeutic agents. Prog. Neurobiol., 82(6):348-360.
[24]Marchi, S., Giorgi, C., Suski, J.M., et al., 2012. Mitochondria-ROS crosstalk in the control of cell death and aging. J. Signal. Transduct., 2012:329635.
[25]McLarnon, J.G., Ryu, J.K., 2008. Relevance of Aβ1–42 intrahippocampal injection as an animal model of inflamed Alzheimer’s disease brain. Curr. Alzheimer Res., 5(5):475-480.
[26]Naaz, H., Singh, S., Pandey, V.P., et al., 2013. Anti-cholinergic alkaloids as potential therapeutic agents for Alzheimer’s disease: an in silico approach. Indian J. Biochem. Biophys., 50(2):120-125.
[27]Neha, Sodhi, R.K., Jaggi, A.S., et al., 2014. Animal models of dementia and cognitive dysfunction. Life Sci., 109(2):73-86.
[28]Peng, S., Zhang, Y., Zhang, J., et al., 2011. Glutamate receptors and signal transduction in learning and memory. Mol. Biol. Rep., 38(1):453-460.
[29]Qin, R.A., Yao, X.X., Huang, Z.Y., 2012. Effects of Compound Danshen Tablets on spatial cognition and expression of brain β-amyloid precursor protein in a rat model of Alzheimer’s disease. J. Tradit. Chin. Med., 32(1):63-66.
[30]Ribeiro, F.M., Camargos, E.R., de Souza, L.C., et al., 2013. Animal models of neurodegenerative diseases. Rev. Bras. Psiquiatr., 35(2):S82-S91.
[31]Sharma, B., Singh, N., 2010. Pitavastatin and 4'-hydroxy-3'-methoxyacetophenone (HMAP) reduce cognitive dysfunction in vascular dementia during experimental diabetes. Curr. Neurovasc. Res., 7(3):180-191.
[32]Singh, M., Kaur, M., Kukreja, H., et al., 2013. Acetylcholinesterase inhibitors as Alzheimer therapy: from nerve toxins to neuroprotection. Eur. J Med. Chem., 70:165-188.
[33]Song, Y., Wang, J., 2010. Overview of Chinese research on senile dementia in mainland China. Ageing Res. Rev., 9(1):S6-S12.
[34]Tamagno, E., Bardini, P., Guglielmotto, M., et al., 2006. The various aggregation states of β-amyloid 1–42 mediate different effects on oxidative stress, neurodegeneration, and BACE-1 expression. Free Radic. Biol. Med., 41(2):202-212.
[35]Wang, N., Chen, X., Geng, D., et al., 2013. Ginkgo biloba leaf extract improves the cognitive abilities of rats with
[36]Wang, X.P., Ding, H.L., 2008. Alzheimer’s disease: epidemiology, genetics, and beyond. Neurosci. Bull., 24(2):105-109.
[37]Wei, H., Li, L., Song, Q., et al., 2005. Behavioural study of the
[38]Wermuth, C.G., 2004. Multitargeted drugs: the end of the “One-target-one-disease” philosophy. Drug Discov. Today, 9(19):826-827.
[39]Wimo, A., Jonsson, L., Bond, J., et al., 2013. The worldwide economic impact of dementia 2010. Alzheimers Dement., 9(1):1-11.e3.
[40]Xie, Q., Tang, Y., Li, W., et al., 2006. Investigation of the binding mode of (−)-meptazinol and bis-meptazinol derivatives on acetylcholinesterase using a molecular docking method. J. Mol. Model., 12(4):390-397.
[41]Yamaguchi, Y., Matsuno, T., Kawashima, S., 2002. Antiamnesic effects of azaindolizinone derivative ZSET845 on impaired learning and decreased ChAT activity induced by amyloid-β 25–35 in the rat. Brain Res., 945(2):259-265.
[42]Zhang, Q., Li, X., Cui, X., et al., 2005.
Open peer comments: Debate/Discuss/Question/Opinion
<1>