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Antioxidant Effect of Barley Sprout Extract via Enhancement of Nuclear Factor-Erythroid 2 Related Factor 2 Activity and Glutathione Synthesis

1
College of Pharmacy, Yonsei University, Incheon 21983, Korea
2
College of Pharmacy, Pusan National University, Busan 46241, Korea
3
Life Science Research Institute, Novarex Co., Ltd., Ochang, Cheongju 28126, Korea
4
Division for Research Center, Dongnam Institute of Radiological and Medical Science, Busan 46033, Korea
5
College of Pharmacy, Chosun University, Gwangju 61452, Korea
6
National Institute of Crop Science(NICS), Rural Development Administration(RDA), Jeollabuk-do 55365, Korea
7
College of Pharmacy, Kyungsung University, Busan 48434, Korea
8
College of Pharmacy, Chungbuk National University, Cheongju 28160, Korea
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Nutrients 2017, 9(11), 1252; https://doi.org/10.3390/nu9111252
Received: 18 September 2017 / Revised: 6 November 2017 / Accepted: 13 November 2017 / Published: 16 November 2017
We previously showed that barley sprout extract (BSE) prevents chronic alcohol intake-induced liver injury in mice. BSE notably inhibited glutathione (GSH) depletion and increased inflammatory responses, revealing its mechanism of preventing alcohol-induced liver injury. In the present study we investigated whether the antioxidant effect of BSE involves enhancing nuclear factor-erythroid 2 related factor 2 (Nrf2) activity and GSH synthesis to inhibit alcohol-induced oxidative liver injury. Mice fed alcohol for four weeks exhibited significantly increased oxidative stress, evidenced by increased malondialdehyde (MDA) level and 4-hydroxynonenal (4-HNE) immunostaining in the liver, whereas treatment with BSE (100 mg/kg) prevented these effects. Similarly, exposure to BSE (0.1–1 mg/mL) significantly reduced oxidative cell death induced by t-butyl hydroperoxide (t-BHP, 300 μM) and stabilized the mitochondrial membrane potential (∆ψ). BSE dose-dependently increased the activity of Nrf2, a potential transcriptional regulator of antioxidant genes, in HepG2 cells. Therefore, increased expression of its target genes, heme oxygenase-1 (HO-1), NADPH quinone oxidoreductase 1 (NQO1), and glutamate-cysteine ligase catalytic subunit (GCLC) was observed. Since GCLC is involved in the rate-limiting step of GSH synthesis, BSE increased the GSH level and decreased both cysteine dioxygenase (CDO) expression and taurine level. Because cysteine is a substrate for both taurine and GSH synthesis, a decrease in CDO expression would further contribute to increased cysteine availability for GSH synthesis. In conclusion, BSE protected the liver cells from oxidative stress by activating Nrf2 and increasing GSH synthesis. View Full-Text
Keywords: barley sprouts; alcohol-induced liver injury; oxidative stress; Nrf2; glutathione barley sprouts; alcohol-induced liver injury; oxidative stress; Nrf2; glutathione
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Lee, Y.-H.; Kim, S.H.; Lee, S.; Kim, K.-M.; Jung, J.-C.; Son, T.G.; Ki, S.H.; Seo, W.-D.; Kwak, J.-H.; Hong, J.T.; Jung, Y.-S. Antioxidant Effect of Barley Sprout Extract via Enhancement of Nuclear Factor-Erythroid 2 Related Factor 2 Activity and Glutathione Synthesis. Nutrients 2017, 9, 1252.

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