Protective effect of Polygonum multiflorum Thunb on amyloid β-peptide 25-35 induced cognitive deficits in mice

Um, Min Young; Choi, Won-Hee; Aan, Ji-Yun; Kim, Sung-Ran; Ha, Tae‐Youl

doi:10.1016/j.jep.2005.08.054

Cited by 86 publications

(60 citation statements)

References 35 publications

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“…As an important lipid peroxidation product, MDA can be considered as an indicator for the oxidative damage extend. Abnormal alteration of MDA content is related to memory impairment, as reported in previous studies (Um et al, 2006). GSH is a sensitive indicator of the ability of a cell or tissue to resist damage.…”

Section: Discussionsupporting

confidence: 69%

The Anti-brain Ageing Effects of Krill Phosphatidylserine in SAMP10 Mice

Wang¹,

Lei²,

Li³

et al. 2012

JAS

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We examined the biological effect of krill phosphatidylserine (K-PS) on brain ageing and investigated the mechanisms that how K-PS works on the brain using senescence-accelerated mouse (SAM) model with age-associated neurodegeneration. SAMP10 mice with 5 months of age were treated orally once a day for 75 days with 10 or 100 mg kg −1 d −1 K-PS (low and high dose). The effect of K-PS treatment on the cross-sectional area and Nissl body number of the neocortex at point C, an area prone to atrophy in SAMP10 mice, behavior and oxidative stress were evaluated by Image-Pro Plus software, step-down testing, and malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) assays. Ionized calcium binding adaptor molecule 1 (Iba-1) and insulin-like growth factor 1 (IGF-1) expression was evaluated using immunohistochemistry. Low or high doses of K-PS significantly increased the cross-sectional area and Nissl body number at point C, partly reversed memory impairment, increased the activity of GSH-Px and reduced MDA levels. Moreover, immunohistochemistry indicated that K-PS suppressed Iba-1 expression and upregulate the expression of IGF-1. These findings suggest that K-PS could prevent or slow the progression of brain atrophy and neuronal damage associated with aging by the inhibition of Iba-1 and the upregulation of IGF-1 expression.

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Section: Discussionsupporting

confidence: 69%

The Anti-brain Ageing Effects of Krill Phosphatidylserine in SAMP10 Mice

Wang¹,

Lei²,

Li³

et al. 2012

JAS

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“…The previous investigations have indicated that intracerebroventricular injection Ab 1-40 could cause memory deficits and lower choline transferase in hippocampus (Stepanichev et al, 2004;Um et al, 2006). As can be seen from Figure 2, our present study demonstrated that intracerebroventricular injection of Ab 1-40 can induce cognitive dysfunction in the MWM test.…”

Section: Psg Improved the Learning And Memory Of Ab 1-40 -Induced Demsupporting

confidence: 78%

Ameliorative effects of physcion 8-O-β-glucopyranoside isolated fromPolygonum cuspidatumon learning and memory in dementia rats induced by Aβ_1–40

Zhou

Zou

et al. 2015

Pharmaceutical Biology

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“…Recently, it was also observed that Ab [25][26][27][28][29][30][31][32][33][34][35] injection activates the glycogen synthase kinase-3b, involved in cell survival regulation, T-phosphorylation and APP processing, suggesting that acute Ab [25][26][27][28][29][30][31][32][33][34][35] injection results in production and seeding of endogenous Ab 1-40/42 and T-phosphorylation (Klementiev et al, 2007). The model therefore appears as highly suitable to analyze the putative antiamnesic and neuroprotective activity of drugs with potential interest in AD, as recently used by several authors (Fang and Liu, 2006;Kuboyama et al, 2006;Meunier et al, 2006;Um et al, 2006;Alkam et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Antiamnesic and Neuroprotective Effects of the Aminotetrahydrofuran Derivative ANAVEX1-41 Against Amyloid β25–35-Induced Toxicity in Mice

Villard

Espallergues

Keller

et al. 2008

Neuropsychopharmacol

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The antiamnesic and neuroprotective activities of the new aminotetrahydrofuran derivative tetrahydro-N,N-dimethyl-5,5-diphenyl-3-furanmethanamine hydrochloride (ANAVEX1-41), a nonselective muscarinic receptor ligand and s 1 protein activator, were examined in mice injected intracerebroventricularly with amyloid b [25][26][27][28][29][30][31][32][33][34][35] ) peptide (9 nmol). Ab 25-35 impaired significantly spontaneous alternation performance, a spatial working memory, and passive avoidance response. When ANAVEX1-41 (1-1000 mg/kg i.p.) was administered 7 days after Ab 25-35 , ie, 20 min before the behavioral tests, it significantly reversed the Ab 25-35 -induced deficits, the most active doses being in the 3-100 mg/kg range. When the compound was preadministered 20 min before Ab 25-35 , ie, 7 days before the tests, it prevented the learning impairments at 30-100 mg/kg. Morphological analysis of corticolimbic structures showed that Ab 25-35 induced a significant cell loss in the CA1 pyramidal cell layer of the hippocampus that was prevented by ANAVEX1-41 (100 mg/kg). Increased number of glial fibrillary acidic protein immunopositive cells in the retrosplenial cortex or throughout the hippocampus revealed an Ab 25-35 -induced inflammation that was prevented by ANAVEX1-41. The drug also prevented the parameters of Ab 25-35 -induced oxidative stress measured in hippocampus extracts, ie, the increases in lipid peroxidation and protein nitration. ANAVEX1-41, however, failed to prevent Ab 25-35 -induced caspase-9 expression. The compound also blocked the Ab 25-35 -induced caspase-3 expression, a marker of apoptosis. Both the muscarinic antagonist scopolamine and the s 1 protein inactivator BD1047 prevented the beneficial effects of ANAVEX1-41 (30 or 100 mg/kg) against Ab 25-35 -induced learning impairments, suggesting that muscarinic and s 1 targets are involved in the drug effect. A synergic effect could indeed account for the very low active doses measured in vivo. These data outline the therapeutic potential of ANAVEX1-41 as a neuroprotective agent in Alzheimer's disease.

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Protective effect of Polygonum multiflorum Thunb on amyloid β-peptide 25-35 induced cognitive deficits in mice

Cited by 86 publications

References 35 publications

The Anti-brain Ageing Effects of Krill Phosphatidylserine in SAMP10 Mice

The Anti-brain Ageing Effects of Krill Phosphatidylserine in SAMP10 Mice

Ameliorative effects of physcion 8-O-β-glucopyranoside isolated fromPolygonum cuspidatumon learning and memory in dementia rats induced by Aβ_1–40

Antiamnesic and Neuroprotective Effects of the Aminotetrahydrofuran Derivative ANAVEX1-41 Against Amyloid β25–35-Induced Toxicity in Mice

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Protective effect of Polygonum multiflorum Thunb on amyloid β-peptide 25-35 induced cognitive deficits in mice

Cited by 86 publications

References 35 publications

The Anti-brain Ageing Effects of Krill Phosphatidylserine in SAMP10 Mice

The Anti-brain Ageing Effects of Krill Phosphatidylserine in SAMP10 Mice

Ameliorative effects of physcion 8-O-β-glucopyranoside isolated fromPolygonum cuspidatumon learning and memory in dementia rats induced by Aβ1–40

Antiamnesic and Neuroprotective Effects of the Aminotetrahydrofuran Derivative ANAVEX1-41 Against Amyloid β25–35-Induced Toxicity in Mice

Contact Info

Product

Resources

About

Ameliorative effects of physcion 8-O-β-glucopyranoside isolated fromPolygonum cuspidatumon learning and memory in dementia rats induced by Aβ_1–40