Boldine treatment protects acetaminophen-induced liver inflammation and acute hepatic necrosis in mice.


Journal

Journal of biochemical and molecular toxicology
ISSN: 1099-0461
Titre abrégé: J Biochem Mol Toxicol
Pays: United States
ID NLM: 9717231

Informations de publication

Date de publication:
Apr 2021
Historique:
revised: 21 10 2020
received: 10 06 2020
accepted: 12 12 2020
pubmed: 5 1 2021
medline: 28 7 2021
entrez: 4 1 2021
Statut: ppublish

Résumé

Drug-induced liver injury (DILI) is a frequent cause responsible for acute liver failure (ALF). Acetaminophen (APAP) is a known hepatotoxin predictably causing intrinsic DILI. At high doses, APAP causes acute liver necrosis and responsible for ALF and liver transplant cases in 50% and 20% of patients, respectively, in the United States alone. Oxidative stress and glutathione depletion are implicated in APAP-induced liver necrosis. Boldine, a plant-derived compound is shown to have promising antioxidant potential. Therefore, this study investigates the protective effect of boldine against APAP-induced acute hepatic necrosis in mice. A single toxic dose of APAP (300 mg/kg b.w. p.o.) was administered in overnight-fasted mice to induce acute liver necrosis. Separately, APAP + boldine and APAP + N-acetylcysteine (NAC) simultaneous treatments were also given. Serum transaminases and reduced glutathione, enzymic antioxidants, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and, IL-6 were evaluated in liver tissue. Acute APAP intoxication significantly elevated serum marker enzymes of hepatotoxicity. APAP administration increased lipid peroxidation, TNF-α, IL-1β, and IL-6 protein expressions. The enzymic antioxidants and reduced glutathione levels were decreased in liver tissue of APAP intoxicated mice. Boldine and NAC simultaneous treatments prevented APAP-induced oxidative stress, inflammation, and necrosis. The results of this study suggest the crucial role of boldine to protect against APAP induced hepatotoxicity by virtue of its antioxidant and anti-inflammatory properties.

Identifiants

pubmed: 33393705
doi: 10.1002/jbt.22697
doi:

Substances chimiques

Aporphines 0
Cytokines 0
Acetaminophen 362O9ITL9D
boldine 8I91GE2769
Acetylcysteine WYQ7N0BPYC

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e22697

Informations de copyright

© 2021 Wiley Periodicals LLC.

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Auteurs

Devaraj Ezhilarasan (D)

Department of Pharmacology, The Blue Lab (Molecular Pharmacology and Toxicology Division), Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences, Chennai, Tamil Nadu, India.
Department of Pharmacology, Biomedical Research Unit and Laboratory Animal Centre, Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences, Chennai, Tamil Nadu, India.

Subramanian Raghunandhakumar (S)

Department of Pharmacology, The Blue Lab (Molecular Pharmacology and Toxicology Division), Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences, Chennai, Tamil Nadu, India.

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