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Quercetin Attenuates Chronic Ethanol-Induced Hepatic Mitochondrial Damage through Enhanced Mitophagy.

ABSTRACT: Emerging evidence suggested mitophagy activation mitigates ethanol-induced liver injury. However, the effect of ethanol on mitophagy is inconsistent. Importantly, the understanding of mitophagy status after chronic ethanol consumption is limited. This study evaluated the effect of quercetin, a naturally-occurring flavonoid, on chronic ethanol-induced mitochondrial damage focused on mitophagy. An ethanol regime to mice for 15 weeks (accounting for 30% of total calories) led to significant mitochondrial damage as evidenced by changes of the mitochondrial ultrastructure, loss of mitochondrial membrane potential and remodeling of membrane lipid composition, which was greatly attenuated by quercetin (100 mg/kg.bw). Moreover, quercetin blocked chronic ethanol-induced mitophagy suppression as denoted by mitophagosomes-lysosome fusion and mitophagy-related regulator elements, including LC3II, Parkin, p62 and voltage-dependent anion channel 1 (VDAC1), paralleling with increased FoxO3a nuclear translocation. AMP-activated protein kinase (AMPK) and extracellular signal regulated kinase 2 (ERK2), instead of AKT and Sirtuin 1, were involved in quercetin-mediated mitophagy activation. Quercetin alleviated ethanol-elicited mitochondrial damage through enhancing mitophagy, highlighting a promising preventive strategy for alcoholic liver disease.

SUBMITTER: Yu X

PROVIDER: S-EPMC4728641 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature

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Quercetin Attenuates Chronic Ethanol-Induced Hepatic Mitochondrial Damage through Enhanced Mitophagy.

Yu Xiao X Xu Yanyan Y Zhang Shanshan S Sun Jian J Liu Peiyi P Xiao Lin L Tang Yuhan Y Liu Liegang L Yao Ping P

Nutrients 20160105 1

Emerging evidence suggested mitophagy activation mitigates ethanol-induced liver injury. However, the effect of ethanol on mitophagy is inconsistent. Importantly, the understanding of mitophagy status after chronic ethanol consumption is limited. This study evaluated the effect of quercetin, a naturally-occurring flavonoid, on chronic ethanol-induced mitochondrial damage focused on mitophagy. An ethanol regime to mice for 15 weeks (accounting for 30% of total calories) led to significant mitocho ...[more]

PMID: 26742072

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Project description:The aim of this study was to investigate the effects of dietary curcumin supplementation on the performance, mitochondrial redox system, mitochondrial DNA (mtDNA) integrity, and antioxidant-related gene expression in the liver of broiler chickens after heat stress treatment. At day 21, a total of 400 Arbor Acres broiler chickens with similar body weight (BW) were divided into 5 groups with 8 replicates per group and then reared either at a normal temperature (22 ± 1 °C) or at a high ambient temperature (34 ± 1 °C for 8 h and 22 ± 1 °C for the remaining time) for 20 d. Broilers in the 5 groups were fed a basal diet at a normal temperature (NT group) and a basal diet with 0, 50, 100, and 200 mg/kg curcumin at a high ambient temperature (HT, CUR50, CUR100, and CUR200 groups), respectively. The serum and liver samples were analyzed for the parameters related to hepatic damage, mitochondrial function, and redox status. The results showed that the G:F was increased in the CUR50 and CUR100 groups, and the final BW was increased in CUR100 group in comparison with the HT group (P < 0.05). When compared with those in the HT group, both serum aspartate and alanine aminotransferase activities were decreased in the curcumin-supplemented groups (P < 0.05). Curcumin decreased the reactive oxygen species (ROS) production but increased the mitochondrial membrane potential in the hepatocytes of the broilers after heat stress (P < 0.05). The broilers in curcumin-supplemented groups had lower malondialdehyde and protein carbonyl concentrations as well as greater thiol concentrations (P < 0.05). The mitochondrial manganese superoxide dismutase (MnSOD) activity in the liver was increased (P < 0.05) in the CUR100 group compared with the HT group. Compared with the heat-stressed broilers, the broilers that were fed curcumin had greater (P < 0.05) mtDNA copy number and ATP concentrations than those in the HT group. Curcumin supplementation attenuated the depression of the thioredoxin 2 and peroxiredoxin-3 gene expressions (P < 0.05). The MnSOD gene expression was increased in the CUR100 and CUR200 groups, and the thioredoxin reductase 2 gene expression was increased in the CUR50 group in comparison with the HT group (P < 0.05). In conclusion, curcumin mitigated the mitochondrial dysfunction in heat-stressed broilers, as evidenced by the suppression of the ROS burst, the maintenance of the thiol pool and mtDNA content, and the enhanced mitochondrial antioxidant gene expression.

Dataset Information

Quercetin Attenuates Chronic Ethanol-Induced Hepatic Mitochondrial Damage through Enhanced Mitophagy.

Publications

Quercetin Attenuates Chronic Ethanol-Induced Hepatic Mitochondrial Damage through Enhanced Mitophagy.

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