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Neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes
In this study, we investigated the effects of streptozotocin-induced type 1 diabetes on antioxidant-like protein-1 immunoreactivity, protein carbonyl levels, and malondialdehyde formation, a marker for lipid peroxidation, in the hippocampus. For this study, streptozotocin (75 mg/kg) was intraperiton...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Medknow Publications & Media Pvt Ltd
2015
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4396109/ https://www.ncbi.nlm.nih.gov/pubmed/25878595 http://dx.doi.org/10.4103/1673-5374.153695 |
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author | Lee, Sang Gun Yoo, Dae Young Jung, Hyo Young Nam, Sung Min Kim, Jong Whi Choi, Jung Hoon Yi, Sun Shin Won, Moo-Ho Yoon, Yeo Sung Hwang, In Koo Moon, Seung Myung |
author_facet | Lee, Sang Gun Yoo, Dae Young Jung, Hyo Young Nam, Sung Min Kim, Jong Whi Choi, Jung Hoon Yi, Sun Shin Won, Moo-Ho Yoon, Yeo Sung Hwang, In Koo Moon, Seung Myung |
author_sort | Lee, Sang Gun |
collection | PubMed |
description | In this study, we investigated the effects of streptozotocin-induced type 1 diabetes on antioxidant-like protein-1 immunoreactivity, protein carbonyl levels, and malondialdehyde formation, a marker for lipid peroxidation, in the hippocampus. For this study, streptozotocin (75 mg/kg) was intraperitoneally injected into adult rats to induce type 1 diabetes. The three experimental parameters were determined at 2, 3, 4 weeks after streptozotocin treatment. Fasting blood glucose levels significantly increased by 20.7–21.9 mM after streptozotocin treatment. The number of antioxidant-like protein-1 immunoreactive neurons significantly decreased in the hippocampal CA1 region, but not the dentate gyrus, 3 weeks after streptozotocin treatment compared to the control group. Malondialdehyde and protein carbonyl levels, which are modified by oxidative stress, significantly increased with a peak at 3 weeks after malondialdehyde treatment, and then decreased 4 weeks after malondialdehyde treatment. These results suggest that neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress 3 weeks after malondialdehyde treatment. |
format | Online Article Text |
id | pubmed-4396109 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Medknow Publications & Media Pvt Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-43961092015-04-15 Neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes Lee, Sang Gun Yoo, Dae Young Jung, Hyo Young Nam, Sung Min Kim, Jong Whi Choi, Jung Hoon Yi, Sun Shin Won, Moo-Ho Yoon, Yeo Sung Hwang, In Koo Moon, Seung Myung Neural Regen Res Research Article In this study, we investigated the effects of streptozotocin-induced type 1 diabetes on antioxidant-like protein-1 immunoreactivity, protein carbonyl levels, and malondialdehyde formation, a marker for lipid peroxidation, in the hippocampus. For this study, streptozotocin (75 mg/kg) was intraperitoneally injected into adult rats to induce type 1 diabetes. The three experimental parameters were determined at 2, 3, 4 weeks after streptozotocin treatment. Fasting blood glucose levels significantly increased by 20.7–21.9 mM after streptozotocin treatment. The number of antioxidant-like protein-1 immunoreactive neurons significantly decreased in the hippocampal CA1 region, but not the dentate gyrus, 3 weeks after streptozotocin treatment compared to the control group. Malondialdehyde and protein carbonyl levels, which are modified by oxidative stress, significantly increased with a peak at 3 weeks after malondialdehyde treatment, and then decreased 4 weeks after malondialdehyde treatment. These results suggest that neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress 3 weeks after malondialdehyde treatment. Medknow Publications & Media Pvt Ltd 2015-03 /pmc/articles/PMC4396109/ /pubmed/25878595 http://dx.doi.org/10.4103/1673-5374.153695 Text en Copyright: © Neural Regeneration Research http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Lee, Sang Gun Yoo, Dae Young Jung, Hyo Young Nam, Sung Min Kim, Jong Whi Choi, Jung Hoon Yi, Sun Shin Won, Moo-Ho Yoon, Yeo Sung Hwang, In Koo Moon, Seung Myung Neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes |
title | Neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes |
title_full | Neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes |
title_fullStr | Neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes |
title_full_unstemmed | Neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes |
title_short | Neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes |
title_sort | neurons in the hippocampal ca1 region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4396109/ https://www.ncbi.nlm.nih.gov/pubmed/25878595 http://dx.doi.org/10.4103/1673-5374.153695 |
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