Combination Effects of Sodium Butyrate and Pyridoxine Treatment on Cell Proliferation and Neuroblast Differentiation in the Dentate Gyrus of d-Galactose-Induced Aging Model Mice

被引：0
作者：
Dae Young Yoo
Woosuk Kim
In Hye Kim
Sung Min Nam
Jin Young Chung
Jung Hoon Choi
Yeo Sung Yoon
Moo-Ho Won
In Koo Hwang
机构：
[1] Seoul National University,Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science
[2] Hallym University,Department of Physiology, College of Medicine
[3] Seoul National University Hospital,Department of Neurology
[4] Kangwon National University,Department of Anatomy, College of Veterinary Medicine
[5] Kangwon National University,Department of Neurobiology, School of Medicine
来源：
Neurochemical Research | 2012年 / 37卷
关键词：
Hippocampus; Aging; Neurogenesis; Histone deacetylase inhibitor; Memory deficit; Vitamin B; Ki67; Doublecortin;
D O I：
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学科分类号：
摘要：
We previously reported that sodium butyrate (SB), a histone deacetylase inhibitor, robustly increased pyridoxine-induced cell proliferation and neuroblast differentiation in the dentate gyrus of the adult mouse. In this study, we investigated the effects of treatment with SB combined with pyridoxine on cell proliferation and neuroblast differentiation in the dentate gyrus of a mouse model of aging induced by d-galactose (d-gal). d-gal was administered to 20-week-old male mice (d-gal mice) for 10 weeks to induce changes that resemble natural aging in animals. Seven weeks after d-gal (100 mg/kg) treatment, vehicle (physiological saline; d-gal-vehicle mice) and SB (300 mg/kg) combined with pyridoxine (Pyr; 350 mg/kg) were administered to the mice (d-gal-Pyr-SB mice) for 3 weeks. Escape latency under water maze in the d-gal mice was longer than that in the control mice. In the d-gal-Pyr-SB mice, escape latency was similar to that in the control mice. In the d-gal mice, many cells in the granule cell layer of the dentate gyrus showed pyknosis and condensation of the cytoplasm. However, in the d-gal-Pyr-SB mice, such cellular changes were rarely found. Furthermore, the d-gal mice showed a great reduction in cell proliferation (Ki67-positive cells) and neuroblast differentiation (doublecortin-positive neuroblasts) in the dentate gyrus compared to control mice. However, in the d-gal-Pyr-SB mice, cell proliferation and neuroblast differentiation were markedly increased in the dentate gyrus. Furthermore, the administration of pyridoxine with sodium butyrate significantly increased Ser133-phosphorylated cyclic AMP response element binding protein in the dentate gyrus. These results indicate that the combination treatment of Pyr with SB in d-gal mice ameliorated the d-gal-induced reduction in cell proliferation, neuroblast differentiation, and memory deficits.
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页码：223 / 231
页数：8
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