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Inhibitory effects of Tabernaemontana divaricata root extract on oxidative stress and neuronal loss induced by amyloid β(25)(–)(35) peptide in mice

In Alzheimer's disease, there are numerous amyloid plaques, neurofibrillary tangles, and neuronal loss in several brain areas. Oxidative stress is involved in the mechanisms of Aβ-peptide induced neurotoxicity by the generation of free radical oxidative stress that may lead to neurodegeneration...

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Autores principales: Khongsombat, Onrawee, nakdook, Walika, ingkaninan, Kornkanok
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5756015/
https://www.ncbi.nlm.nih.gov/pubmed/29322008
http://dx.doi.org/10.1016/j.jtcme.2017.05.009
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author Khongsombat, Onrawee
nakdook, Walika
ingkaninan, Kornkanok
author_facet Khongsombat, Onrawee
nakdook, Walika
ingkaninan, Kornkanok
author_sort Khongsombat, Onrawee
collection PubMed
description In Alzheimer's disease, there are numerous amyloid plaques, neurofibrillary tangles, and neuronal loss in several brain areas. Oxidative stress is involved in the mechanisms of Aβ-peptide induced neurotoxicity by the generation of free radical oxidative stress that may lead to neurodegeneration. Tabernaemontana divaricata has various medical properties in Thai folklore medicine including prevent forgetfulness or improve memory. The present study aimed to investigate the effects of T. divaricata root extract (TDE) on Aβ(25)(–)(35) peptides induced neuronal loss and oxidative stress in mice. Male ICR mice were administered with vehicle or TDE (250, 500, and 1000 mg/kg b.w., p.o.) for 28 consecutive days. Then, these mice were given a single intracerebroventricular (i.c.v.) injection of Aβ(25)(–)(35) or phosphate buffer saline (PBS) (10 μg/mouse). The novel object recognition (NOR) test was used to determine memory disturbance. In addition, the neuronal cells in the cerebral cortex and hippocampus were measured by using crystal violet staining and lipid peroxidation was determined by measuring the formation of thiobarbituric acid reactive substances. An i.c.v. injection of Aβ(25)(–)(35) peptides could significantly induce memory impairment, increase level of lipid peroxidation including the neuronal loss in CA3 of hippocampus. However, the mice pretreated with TDE could prevent the memory loss, neuronal loss and decrease lipid peroxidation. These results suggest the potential therapeutic value in dementia of TDE through its antioxidant property.
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spelling pubmed-57560152018-01-10 Inhibitory effects of Tabernaemontana divaricata root extract on oxidative stress and neuronal loss induced by amyloid β(25)(–)(35) peptide in mice Khongsombat, Onrawee nakdook, Walika ingkaninan, Kornkanok J Tradit Complement Med Original Article In Alzheimer's disease, there are numerous amyloid plaques, neurofibrillary tangles, and neuronal loss in several brain areas. Oxidative stress is involved in the mechanisms of Aβ-peptide induced neurotoxicity by the generation of free radical oxidative stress that may lead to neurodegeneration. Tabernaemontana divaricata has various medical properties in Thai folklore medicine including prevent forgetfulness or improve memory. The present study aimed to investigate the effects of T. divaricata root extract (TDE) on Aβ(25)(–)(35) peptides induced neuronal loss and oxidative stress in mice. Male ICR mice were administered with vehicle or TDE (250, 500, and 1000 mg/kg b.w., p.o.) for 28 consecutive days. Then, these mice were given a single intracerebroventricular (i.c.v.) injection of Aβ(25)(–)(35) or phosphate buffer saline (PBS) (10 μg/mouse). The novel object recognition (NOR) test was used to determine memory disturbance. In addition, the neuronal cells in the cerebral cortex and hippocampus were measured by using crystal violet staining and lipid peroxidation was determined by measuring the formation of thiobarbituric acid reactive substances. An i.c.v. injection of Aβ(25)(–)(35) peptides could significantly induce memory impairment, increase level of lipid peroxidation including the neuronal loss in CA3 of hippocampus. However, the mice pretreated with TDE could prevent the memory loss, neuronal loss and decrease lipid peroxidation. These results suggest the potential therapeutic value in dementia of TDE through its antioxidant property. Elsevier 2017-06-16 /pmc/articles/PMC5756015/ /pubmed/29322008 http://dx.doi.org/10.1016/j.jtcme.2017.05.009 Text en © 2018 Center for Food and Biomolecules, National Taiwan University. Production and hosting by Elsevier Taiwan LLC. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Original Article
Khongsombat, Onrawee
nakdook, Walika
ingkaninan, Kornkanok
Inhibitory effects of Tabernaemontana divaricata root extract on oxidative stress and neuronal loss induced by amyloid β(25)(–)(35) peptide in mice
title Inhibitory effects of Tabernaemontana divaricata root extract on oxidative stress and neuronal loss induced by amyloid β(25)(–)(35) peptide in mice
title_full Inhibitory effects of Tabernaemontana divaricata root extract on oxidative stress and neuronal loss induced by amyloid β(25)(–)(35) peptide in mice
title_fullStr Inhibitory effects of Tabernaemontana divaricata root extract on oxidative stress and neuronal loss induced by amyloid β(25)(–)(35) peptide in mice
title_full_unstemmed Inhibitory effects of Tabernaemontana divaricata root extract on oxidative stress and neuronal loss induced by amyloid β(25)(–)(35) peptide in mice
title_short Inhibitory effects of Tabernaemontana divaricata root extract on oxidative stress and neuronal loss induced by amyloid β(25)(–)(35) peptide in mice
title_sort inhibitory effects of tabernaemontana divaricata root extract on oxidative stress and neuronal loss induced by amyloid β(25)(–)(35) peptide in mice
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5756015/
https://www.ncbi.nlm.nih.gov/pubmed/29322008
http://dx.doi.org/10.1016/j.jtcme.2017.05.009
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