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Article

Allyl Isothiocyanate Protects Acetaminophen-Induced Liver Injury via NRF2 Activation by Decreasing Spontaneous Degradation in Hepatocyte

by
Min Woo Kim
1,
Ju-Hee Kang
2,
Hyun Jin Jung
2,
Se Yong Park
1,
Thu Han Le Phan
2,
Hee Namgung
3,
Seung-Yong Seo
2,
Yeo Sung Yoon
1,*,† and
Seung Hyun Oh
2,*,†
1
Department of Anatomy and Cell Biology, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea
2
College of Pharmacy, Gachon University, Incheon 21936, Korea
3
Department of Health Sciences and Technology, GAIHST, Gachon University, Incheon 21999, Korea
*
Authors to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Nutrients 2020, 12(11), 3585; https://doi.org/10.3390/nu12113585
Submission received: 30 September 2020 / Revised: 13 November 2020 / Accepted: 19 November 2020 / Published: 23 November 2020
(This article belongs to the Special Issue Natural Products and Human Health: Current Understanding and Application)
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Abstract

Acetaminophen (APAP) is one of the most frequently prescribed analgesic and anti-pyretic drugs. However, APAP-induced hepatotoxicity is a major cause of acute liver failure globally. While the therapeutic dose is safe, an overdose of APAP produces an excess of the toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI), subsequently resulting in hepatotoxicity. Allyl isothiocyanate (AITC), a bioactive molecule in cruciferous plants, is reported to exert various biological effects, including anti-inflammatory, anti-cancer, and anti-microbial effects. Notably, AITC is known for activating nuclear factor erythroid 2-related factor 2 (NRF2), but there is limited evidence supporting the beneficial effects on hepatocytes and liver, where AITC is mainly metabolized. We applied a mouse model in the current study to investigate whether AITC protects the liver against APAP-induced injury, wherein we observed the protective effects of AITC. Furthermore, NRF2 nuclear translocation and the increase of target genes by AITC treatment were confirmed by in vitro experiments. APAP-induced cell damage was attenuated by AITC via an NRF2-dependent manner, and rapid NRF2 activation by AITC was attributed to the elevation of NRF2 stability by decreasing its spontaneous degradation. Moreover, liver tissues from our mouse experiment revealed that AITC increases the expression of heme oxygenase-1 (HO-1), an NRF2 target gene, confirming the potential of AITC as a hepatoprotective agent that induces NRF2 activation. Taken together, our results indicate the potential of AITC as a natural-product-derived NRF2 activator targeting the liver.
Keywords: allyl isothiocyanate (AITC); NRF2; acetaminophen (APAP; N-acetyl-p-aminophenol); hepatotoxicity allyl isothiocyanate (AITC); NRF2; acetaminophen (APAP; N-acetyl-p-aminophenol); hepatotoxicity

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MDPI and ACS Style

Kim, M.W.; Kang, J.-H.; Jung, H.J.; Park, S.Y.; Phan, T.H.L.; Namgung, H.; Seo, S.-Y.; Yoon, Y.S.; Oh, S.H. Allyl Isothiocyanate Protects Acetaminophen-Induced Liver Injury via NRF2 Activation by Decreasing Spontaneous Degradation in Hepatocyte. Nutrients 2020, 12, 3585. https://doi.org/10.3390/nu12113585

AMA Style

Kim MW, Kang J-H, Jung HJ, Park SY, Phan THL, Namgung H, Seo S-Y, Yoon YS, Oh SH. Allyl Isothiocyanate Protects Acetaminophen-Induced Liver Injury via NRF2 Activation by Decreasing Spontaneous Degradation in Hepatocyte. Nutrients. 2020; 12(11):3585. https://doi.org/10.3390/nu12113585

Chicago/Turabian Style

Kim, Min Woo, Ju-Hee Kang, Hyun Jin Jung, Se Yong Park, Thu Han Le Phan, Hee Namgung, Seung-Yong Seo, Yeo Sung Yoon, and Seung Hyun Oh. 2020. "Allyl Isothiocyanate Protects Acetaminophen-Induced Liver Injury via NRF2 Activation by Decreasing Spontaneous Degradation in Hepatocyte" Nutrients 12, no. 11: 3585. https://doi.org/10.3390/nu12113585

APA Style

Kim, M. W., Kang, J.-H., Jung, H. J., Park, S. Y., Phan, T. H. L., Namgung, H., Seo, S.-Y., Yoon, Y. S., & Oh, S. H. (2020). Allyl Isothiocyanate Protects Acetaminophen-Induced Liver Injury via NRF2 Activation by Decreasing Spontaneous Degradation in Hepatocyte. Nutrients, 12(11), 3585. https://doi.org/10.3390/nu12113585

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