Sirtuin-3 activation by honokiol restores mitochondrial dysfunction in the hippocampus of the hepatic encephalopathy rat model of ammonia neurotoxicity.
SIRT3
ammonia neurotoxicity
honokiol
mitochondrial derangements
moderate-grade hepatic encephalopathy
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:
May 2021
May 2021
Historique:
revised:
06
11
2020
received:
17
07
2020
accepted:
20
01
2021
pubmed:
2
2
2021
medline:
29
7
2021
entrez:
1
2
2021
Statut:
ppublish
Résumé
The neurotoxic level of ammonia in the brain during liver cirrhosis causes a nervous system disorder, hepatic encephalopathy (HE), by affecting mitochondrial functions. Sirtuin-3 (SIRT3) is emerging as a master regulator of mitochondrial integrity, which is currently being focused as a pathogenic hotspot for HE. This article describes SIRT3 level versus mitochondrial dysfunction markers in the hippocampus of the control, the moderate-grade hepatic encephalopathy (MoHE), developed in thioacetamide-induced (100 mg/kg bw ip for 10 days) liver cirrhotic rats, and the MoHE rats treated with an SIRT3 activator, honokiol (HKL; 10 mg/kg bw ip), for 7 days from 8th day of the thioacetamide schedule. As compared with the control group rats, hippocampus mitochondria of MoHE rats showed a significant decline in SIRT3 expression and its activity with concordant enhancement of ROS and declined membrane permeability transition and organelle viability scores. This was consistent with the declined mitochondrial thiol level and thiol-regenerating enzyme, isocitrate dehydrogenase 2. Also, significantly declined activities of electron transport chain complexes I, III, IV, and Q
Substances chimiques
SIRT3 protein, rat
0
Ammonia
7664-41-7
Sirtuins
EC 3.5.1.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e22735Subventions
Organisme : DST-SERB Govt India
ID : EMR/2016/006501
Informations de copyright
© 2021 Wiley Periodicals LLC.
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