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Neuroprotective effects of dehydroglyasperin C through increased expression of heme oxygenase-1 in mouse hippocampal cells

Published online by Cambridge University Press:  19 October 2012

Hyo Jung Kim ,
Soon Sung Lim ,
In Sil Park ,
Choon Hwan Lee  and
Jong-Sang Kim
Hyo Jung Kim
Affiliation:
School of Food Science and Biotechnology, Kyungpook National University, Daegu, South Korea
Soon Sung Lim
Affiliation:
Department of Food Science and Nutrition, Hallym University, Chuncheon 200–702, Republic of Korea
In Sil Park
Affiliation:
School of Food Science and Biotechnology, Kyungpook National University, Daegu, South Korea
Choon Hwan Lee
Affiliation:
Department of Bioscience and Biotechnology and Bio/Molecular Informatics Center, Konkuk University, Seoul, South Korea
Jong-Sang Kim
Affiliation:
School of Food Science and Biotechnology, Kyungpook National University, Daegu, South Korea
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Abstract

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Proceedings of the Nutrition Society , Volume 71 , Issue OCE2: Summer Meeting hosted by the Irish Section, 16–19 July 2012, Translational nutrition: integrating research, practice and policy , 2012 , E117
Copyright
Copyright © The Authors 2012

Licorice, the root of the Glycyrrhiza species (Glycyrrhiza uralensis Fisher), is known to have antioxidant, anti-inflammatory, anti-viral, and anti-tumor properties( Reference Seo, Lee and Kim 1 , Reference Shibata 2 ). The objective of this study was to explore the neuroprotective effect of dehydroglyasperin C (DGC) against glutamate-induced oxidative stress in the mouse hippocampal HT22 cells. DGC significantly reduced cytotoxicity and reactive oxygen species (ROS) generation induced by glutamate in HT22 cells, whereas DGC did not restore glutathione depletion caused by glutamate. In addition, we investigated further whether DGC affected the expression of heme oxygenase (HO)-1, one of major cellular antioxidant defense systems, and found that DGC dose-dependently increased HO-1 expression. DGC-mediated cytoprotection of HT22 neuronal cells from glutamate insult was abrogated by either HO-1 inhibitor (Tin protoporphyrin, SnPP) or AKT inhibitor (LY294002). In conclusion, the present results demonstrate for the first time that DGC protects neuronal cells against glutamate-induced oxidative injury through the induction of HO-1 expression which is, in turn, activated maybe through Nrf2-Keap1 and PI3K/AKT signaling pathways.

Figure 1. Effect of glutamate, DGC, Trolox on proliferation of mouse neuroblastoma HT22 cells.

This work was supported by the National Research Foundation of Korea Grant funded by the Korean Government (MEST)” (NRF-2010-00272, 2011-0009782)

References

1. Seo, JY, Lee, YS & Kim, HJ et al. (2010) Dehydroglyasperin C isolated from licorice caused Nrf2-mediated induction of detoxifying enzymes. J Agric Food Chem 58, 1603–1608.CrossRefGoogle ScholarPubMed
2. Shibata, S (2000) A drug over the millennia: pharmacognosy, chemistry, and pharmacology of licorice. Yakugaku Zasshi 120, 849–862.CrossRefGoogle ScholarPubMed
Figure 0

Figure 1. Effect of glutamate, DGC, Trolox on proliferation of mouse neuroblastoma HT22 cells.