SIRT1 alleviates isoniazid-induced hepatocyte injury by reducing histone acetylation in the IL-6 promoter region.


Journal

International immunopharmacology
ISSN: 1878-1705
Titre abrégé: Int Immunopharmacol
Pays: Netherlands
ID NLM: 100965259

Informations de publication

Date de publication:
Feb 2019
Historique:
received: 06 09 2018
revised: 20 11 2018
accepted: 30 11 2018
pubmed: 24 12 2018
medline: 10 5 2019
entrez: 23 12 2018
Statut: ppublish

Résumé

Silent information regulator 1 (SIRT1) is a type III histone deacetylase that is related to the inhibition of the inflammatory response. The aim of this study was to investigate the regulation of SIRT1 on isoniazid-induced hepatocyte injury and the possible mechanism of histone modification. We found that compared with the blank control group, expression of SIRT1 was decreased in the isoniazid group and that expression of NF-κB p65 was increased, leading to an increase of the expression of inflammatory cytokines Interleukin-6 (IL-6) and Tumour necrosis factor alpha (TNF-α). The level of histone H3K9 acetylation in the promoter region of IL-6 was increased as well. Addition of a SIRT1 agonist (SRT1720) alleviated the inflammatory reaction caused by isoniazid, while the use of a SIRT1 inhibitor (EX527) aggravated the inflammatory damage to cells. In conclusion, these findings indicated that during the period of isoniazid-induced hepatocyte injury, SIRT1 levels were decreased and inflammatory factor levels were increased. Activation of SIRT1 may reduce hepatocyte injury by reducing the level of histone H3K9 acetylation in the promoter region of the IL-6 gene.

Identifiants

pubmed: 30578970
pii: S1567-5769(18)30577-0
doi: 10.1016/j.intimp.2018.11.054
pii:
doi:

Substances chimiques

6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide 0
Antitubercular Agents 0
Carbazoles 0
Heterocyclic Compounds, 4 or More Rings 0
Histones 0
Interleukin-6 0
RNA, Messenger 0
SRT1720 0
SIRT1 protein, human EC 3.5.1.-
Sirtuin 1 EC 3.5.1.-
Isoniazid V83O1VOZ8L

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

348-355

Informations de copyright

Copyright © 2018 Elsevier B.V. All rights reserved.

Auteurs

Yiyang Zhang (Y)

School of Public Health, North China University of Science and Technology, No. 21 Bohai Road, Caofeidian Eco-city, Tangshan, Hebei 063210, PR China.

Yingshu Li (Y)

School of Public Health, North China University of Science and Technology, No. 21 Bohai Road, Caofeidian Eco-city, Tangshan, Hebei 063210, PR China.

Jinfeng Li (J)

School of Public Health, North China University of Science and Technology, No. 21 Bohai Road, Caofeidian Eco-city, Tangshan, Hebei 063210, PR China.

Biao Li (B)

School of Public Health, North China University of Science and Technology, No. 21 Bohai Road, Caofeidian Eco-city, Tangshan, Hebei 063210, PR China.

Yingzhi Chong (Y)

School of Public Health, North China University of Science and Technology, No. 21 Bohai Road, Caofeidian Eco-city, Tangshan, Hebei 063210, PR China.

Guoying Zheng (G)

School of Public Health, North China University of Science and Technology, No. 21 Bohai Road, Caofeidian Eco-city, Tangshan, Hebei 063210, PR China.

Shufeng Sun (S)

School of Public Health, North China University of Science and Technology, No. 21 Bohai Road, Caofeidian Eco-city, Tangshan, Hebei 063210, PR China.

Fumin Feng (F)

School of Public Health, North China University of Science and Technology, No. 21 Bohai Road, Caofeidian Eco-city, Tangshan, Hebei 063210, PR China. Electronic address: fm_feng@sina.com.

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Classifications MeSH