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Article: S-allylmercaptocysteine improves nonalcoholic steatohepatitis by enhancing AHR/NRF2-mediated drug metabolising enzymes and reducing NF-κB/IκBα and NLRP3/6-mediated inflammation

TitleS-allylmercaptocysteine improves nonalcoholic steatohepatitis by enhancing AHR/NRF2-mediated drug metabolising enzymes and reducing NF-κB/IκBα and NLRP3/6-mediated inflammation
Authors
KeywordsS-allylmercaptocysteine
NASH
Inflammasome
Antioxidant responses
Xenobiotic responses
Issue Date2021
PublisherSpringer (part of Springer Nature). The Journal's web site is located at http://www.springer.com/steinkopff/journal/394
Citation
European Journal of Nutrition, 2021, v. 60 n. 2, p. 961-973 How to Cite?
AbstractPurpose: To investigate the novel molecular mechanisms of the antioxidant and anti-inflammatory properties of S-allylmercaptocysteine (SAMC) based on a transcriptomic study in a nonalcoholic steatohepatitis (NASH) rat model Methods: NASH was induced in Sprague–Dawley rats by feeding with a high fat diet (HFD) for 12 weeks. 200 mg/kg SAMC was fed by oral gavage for 4 weeks from 9 to 12 week. Results: SAMC co-administration attenuated HFD-induced liver injury, including the increased serum ALT, hepatic oxidative stress and inflammation. Transcriptomic analysis revealed that SAMC dramatically induced the XRE- and ARE-driven drug metabolising enzymes (DMEs) including Akr7a3, Akr1b8, and Nqo1. The nuclear translocation of the upstream regulator of xenobiotics metabolism, AHR, and regulator of antioxidant responses, NRF2, were significantly increased by SAMC treatment. Furthermore, SAMC counteracted the effects of HFD on NF-κB/IκB and NLRP3/6 pathways with decreasing protein levels of ASC, cleaved caspase-1, IL-18, and IL-1β. These results were further verified in another mice NASH model induced by an MCD diet with SAMC co-administration. Conclusion: We propose that SAMC triggers AHR/NRF2-mediated antioxidant responses which may further suppress the NLRP3/6 inflammasome pathway and NF-κB activation, contributing to the improvement of NASH.
Persistent Identifierhttp://hdl.handle.net/10722/285415
ISSN
2023 Impact Factor: 4.1
2023 SCImago Journal Rankings: 1.167
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYu, Q-
dc.contributor.authorLee, YY-
dc.contributor.authorXia, Z-
dc.contributor.authorLiong, EC-
dc.contributor.authorXiao, J-
dc.contributor.authorTipoe, GL-
dc.date.accessioned2020-08-18T03:53:13Z-
dc.date.available2020-08-18T03:53:13Z-
dc.date.issued2021-
dc.identifier.citationEuropean Journal of Nutrition, 2021, v. 60 n. 2, p. 961-973-
dc.identifier.issn1436-6207-
dc.identifier.urihttp://hdl.handle.net/10722/285415-
dc.description.abstractPurpose: To investigate the novel molecular mechanisms of the antioxidant and anti-inflammatory properties of S-allylmercaptocysteine (SAMC) based on a transcriptomic study in a nonalcoholic steatohepatitis (NASH) rat model Methods: NASH was induced in Sprague–Dawley rats by feeding with a high fat diet (HFD) for 12 weeks. 200 mg/kg SAMC was fed by oral gavage for 4 weeks from 9 to 12 week. Results: SAMC co-administration attenuated HFD-induced liver injury, including the increased serum ALT, hepatic oxidative stress and inflammation. Transcriptomic analysis revealed that SAMC dramatically induced the XRE- and ARE-driven drug metabolising enzymes (DMEs) including Akr7a3, Akr1b8, and Nqo1. The nuclear translocation of the upstream regulator of xenobiotics metabolism, AHR, and regulator of antioxidant responses, NRF2, were significantly increased by SAMC treatment. Furthermore, SAMC counteracted the effects of HFD on NF-κB/IκB and NLRP3/6 pathways with decreasing protein levels of ASC, cleaved caspase-1, IL-18, and IL-1β. These results were further verified in another mice NASH model induced by an MCD diet with SAMC co-administration. Conclusion: We propose that SAMC triggers AHR/NRF2-mediated antioxidant responses which may further suppress the NLRP3/6 inflammasome pathway and NF-κB activation, contributing to the improvement of NASH.-
dc.languageeng-
dc.publisherSpringer (part of Springer Nature). The Journal's web site is located at http://www.springer.com/steinkopff/journal/394-
dc.relation.ispartofEuropean Journal of Nutrition-
dc.subjectS-allylmercaptocysteine-
dc.subjectNASH-
dc.subjectInflammasome-
dc.subjectAntioxidant responses-
dc.subjectXenobiotic responses-
dc.titleS-allylmercaptocysteine improves nonalcoholic steatohepatitis by enhancing AHR/NRF2-mediated drug metabolising enzymes and reducing NF-κB/IκBα and NLRP3/6-mediated inflammation-
dc.typeArticle-
dc.identifier.emailTipoe, GL: tgeorge@hku.hk-
dc.identifier.authorityTipoe, GL=rp00371-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s00394-020-02305-1-
dc.identifier.pmid32556446-
dc.identifier.scopuseid_2-s2.0-85086701824-
dc.identifier.hkuros312702-
dc.identifier.volume60-
dc.identifier.issue2-
dc.identifier.spage961-
dc.identifier.epage973-
dc.identifier.isiWOS:000541100000001-
dc.publisher.placeGermany-
dc.identifier.issnl1436-6207-

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