Improvement of Impaired Memory in Mice by Schisandrin

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Abstract:

We assessed the effectiveness and mechanism of action of schisandrin on modulation of learning and memory disorders in mice. Memory impairment was established in mice by intraperitoneal injection of pentobarbital sodium (20 mg/kg). Schisandrin (0.5, 1.0, 2.0g/kg) were administered by intragavage once daily for 14 consecutive days. The Morris water maze test was used to evaluate the ability of schisandrin to reduce phenobarbital-induced learning and memory impairment. The levels of superoxide dismutase (SOD) nitric oxide (NO) and catalase (CAT) were measured in brain tissue samples taken from the mice. Other biomarkers measured included expression of nuclear transcription factor-kappa-B (NF-κB) and brain-derived neurotrophic factor (BDNF) in the hippocampus CA1 region, which were determined by immunohistochemical analysis. On the fifth day of treatment, the mice in the pentobarbital sodium group performed worse on the Morris water maze test compared to untreated controls (P<0.01), which could be prolonged after schisandrin treatment (P<0.05 for="" low="" and="" intermediate="" dose="" groups="" analysis="" of="" brain="" tissues="" showed="" that="" compared="" with="" the="" control="" group="" no="" levels="" were="" increased="" sod="" cat="" activity="" decreased="" in="" pentobarbital="" sodium="" i="">P<0.01). After treatment with schisandrin, the NO levels were significantly decreased (P<0.01), while SOD and CAT activity increased (P<0.01). Immunohistochemistry analysis showed that, in phenobarbital only group, the protein expression of BDNF decreased, NF-κB increased compared to untreated controls, and schisandrin could reverse this trend (P<0.05 and="" i="">P<0.01, respectively). The results suggest that schisandrin is effective in improving the learning and memory deficiency induced by pentobarbital sodium, the mechanism of which may be related modulation of cellular response to oxidative stress.

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Advanced Materials Research (Volumes 750-752)

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1533-1538

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August 2013

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© 2013 Trans Tech Publications Ltd. All Rights Reserved

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[1] Huang ZS, Liu MP, Chen CZ. 1997. Studies on improving the ability of learning and memories of yangshoudan. Zhong guo Zhong Xi Yi Jie He Za Zhi. 17(9): 553-556.

Google Scholar

[2] Xv S Y, Bian R L, Chen X. 2002. Experimental methods in Pharmacology (3th Ed,Beijing) People's Medical Publishing House: 226-334.

Google Scholar

[3] Matsushita A, Kawasaki K, Matsubara K, Eigyo M, Shindo H, Takada S. 1988. Activation of brain function by S-135, a benzodiazepine receptor inverse agonist. Prog Neuropsychopharmacol Biol Psychiatry. 12(6): 951-66.

DOI: 10.1016/0278-5846(88)90091-7

Google Scholar

[4] Monfils MH, Cowansage KK, LeDoux JE. 2007. Brain-derived neurotrophic factor: linking fear learning to memory consolidation. Mol Pharmacol. Aug, 72(2): 235-7.

DOI: 10.1124/mol.107.038232

Google Scholar

[5] Cantuti CI, Shukitt-Hale B, Joseph JA. 2000. Neurobehavioural aspects of antioxidants in aging. Int J Dev Neurosci 18: 367–381.

DOI: 10.1016/s0736-5748(00)00008-3

Google Scholar

[6] Grech ED, Dodd NJF, Lackson MJ, Morrison WL, Faragher EB, Ramsdale DR. 1996. Evidence for free radical generation after primary percutaneous transluminal angioplasty recanalization in acute myocardial infarction. Am J Cardiol 77: 122–127.

DOI: 10.1016/s0002-9149(96)90580-9

Google Scholar

[7] Massaad C A, Washington T M, Pautler R G, et al. 2009, Overexpression of SOD-2 reduces hippocampal superoxide and prevents memory deficits in a mouse model of Alzheimer's disease . Proc Natl Acad Sci U S A, 106(32): 13576–13581.

DOI: 10.1073/pnas.0902714106

Google Scholar

[8] Clausen A, Doctrow S, Baudry M., 2010 . Prevention of cognitive deficits and brain oxidative stress with superoxide dismutase/catalase mimetics in aged mice. Neurobiol Aging. 31(3): 425-33.

DOI: 10.1016/j.neurobiolaging.2008.05.009

Google Scholar

[9] Contestabile A. 2008. Regulation of transcription factors by nitric oxide in neurons and in neural-derived tumor cells. Prog Neurobiol. 84(4): 317-28.

DOI: 10.1016/j.pneurobio.2008.01.002

Google Scholar

[10] Valen G, Yan ZQ, Hansson GK. 2001. Nuclear factor Kappa-B and theheart. J Am Coll Cardiol 2: 307–314.

Google Scholar

[11] Kumar A, Takada Y, Boriek AM, Aggarwal BB. 2004. Nuclear factor-kappaB: its role in health and disease. J Mol Med 82: 434–448.

DOI: 10.1007/s00109-004-0555-y

Google Scholar

[12] Pardon M C., 2010. Role of neurotrophic factors in behavioral processes: implications for the treatment of psychiatric and neurodegenerative disorders. Vitam Horm, 82: 185-200.

Google Scholar

[13] Ogonovszky H, Berkes I, Kumagai S, Kaneko T, Tahara S, Goto S, Radák Z, 2005, The effects of moderate-, strenuous- and over-training on oxidative stress markers, DNA repair, and memory, in rat brain. Neurochem Int, 46(8): 635-640.

DOI: 10.1016/j.neuint.2005.02.009

Google Scholar