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Nutrients. 2019 Jan 15;11(1). pii: E176. doi: 10.3390/nu11010176.

Ascorbic Acid Mitigates D-galactose-Induced Brain Aging by Increasing Hippocampal Neurogenesis and Improving Memory Function.

Author information

1
Department of Anatomy, College of Veterinary Medicine, Konkuk University, Seoul 05029, Korea. skavet@konkuk.ac.kr.
2
Center for Neuroscience, Korea Institute of Science and Technology, Seoul 02792, Korea. misun@kist.re.kr.
3
Department of Anatomy, College of Veterinary Medicine, Konkuk University, Seoul 05029, Korea. phoenix_1st@naver.com.
4
Center for Neuroscience, Korea Institute of Science and Technology, Seoul 02792, Korea. hrhim@kist.re.kr.
5
Department of Anatomy, College of Veterinary Medicine, Konkuk University, Seoul 05029, Korea. ssnahm@konkuk.ac.kr.
6
Department of Science in Korean Medicine, Brain Korea 21 Plus Program, Kyung Hee University, Seoul 02447, Korea. ihcho@khu.ac.kr.
7
Department of Cancer Preventive Material Development, Graduate School, Kyung Hee University, Seoul 02447, Korea. ihcho@khu.ac.kr.
8
Department of Anatomy, College of Veterinary Medicine, Konkuk University, Seoul 05029, Korea. bjchang@konkuk.ac.kr.
9
Ginsentology Research Laboratory and Department of Physiology, College of Veterinary Medicine, Konkuk University, Seoul 05029, Korea. hyunjoongk@gmail.com.
10
Ginsentology Research Laboratory and Department of Physiology, College of Veterinary Medicine, Konkuk University, Seoul 05029, Korea. vettman@konkuk.ac.kr.
11
Ginsentology Research Laboratory and Department of Physiology, College of Veterinary Medicine, Konkuk University, Seoul 05029, Korea. synah@konkuk.ac.kr.

Abstract

Ascorbic acid is essential for normal brain development and homeostasis. However, the effect of ascorbic acid on adult brain aging has not been determined. Long-term treatment with high levels of D-galactose (D-gal) induces brain aging by accumulated oxidative stress. In the present study, mice were subcutaneously administered with D-gal (150 mg/kg/day) for 10 weeks; from the seventh week, ascorbic acid (150 mg/kg/day) was orally co-administered for four weeks. Although D-gal administration alone reduced hippocampal neurogenesis and cognitive functions, co-treatment of ascorbic acid with D-gal effectively prevented D-gal-induced reduced hippocampal neurogenesis through improved cellular proliferation, neuronal differentiation, and neuronal maturation. Long-term D-gal treatment also reduced expression levels of synaptic plasticity-related markers, i.e., synaptophysin and phosphorylated Ca2+/calmodulin-dependent protein kinase II, while ascorbic acid prevented the reduction in the hippocampus. Furthermore, ascorbic acid ameliorated D-gal-induced downregulation of superoxide dismutase 1 and 2, sirtuin1, caveolin-1, and brain-derived neurotrophic factor and upregulation of interleukin 1 beta and tumor necrosis factor alpha in the hippocampus. Ascorbic acid-mediated hippocampal restoration from D-gal-induced impairment was associated with an enhanced hippocampus-dependent memory function. Therefore, ascorbic acid ameliorates D-gal-induced impairments through anti-oxidative and anti-inflammatory effects, and it could be an effective dietary supplement against adult brain aging.

KEYWORDS:

D-galactose; ascorbic acid; brain aging; hippocampus; neurogenesis

PMID:
30650605
PMCID:
PMC6356429
DOI:
10.3390/nu11010176
[Indexed for MEDLINE]
Free PMC Article

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