The role of oxidative stress in alcoholic fatty liver disease : a systematic review and meta-analysis of preclinical studies.

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MetadadosDescriçãoIdioma
Autor(es): dc.creatorRabelo, Ana Carolina Silveira-
Autor(es): dc.creatorAndrade, Amanda Kelly de Lima-
Autor(es): dc.creatorCosta, Daniela Caldeira-
Data de aceite: dc.date.accessioned2025-08-21T15:11:01Z-
Data de disponibilização: dc.date.available2025-08-21T15:11:01Z-
Data de envio: dc.date.issued2025-02-27-
Data de envio: dc.date.issued2023-
Fonte completa do material: dc.identifierhttps://www.repositorio.ufop.br/handle/123456789/19807-
Fonte completa do material: dc.identifierhttps://doi.org/10.3390/nu16081174-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/capes/1004729-
Descrição: dc.descriptionAlcoholic Fatty Liver Disease (AFLD) is characterized by the accumulation of lipids in liver cells owing to the metabolism of ethanol. This process leads to a decrease in the NAD+/NADH ratio and the generation of reactive oxygen species. A systematic review and meta-analysis were conducted to investigate the role of oxidative stress in AFLD. A total of 201 eligible manuscripts were included, which revealed that animals with AFLD exhibited elevated expression of CYP2E1, decreased enzymatic activity of antioxidant enzymes, and reduced levels of the transcription factor Nrf2, which plays a pivotal role in the synthesis of antioxidant enzymes. Furthermore, animals with AFLD exhibited increased levels of lipid peroxidation markers and carbonylated proteins, collectively contributing to a weakened antioxidant defense and increased oxidative damage. The liver damage in AFLD was supported by significantly higher activity of alanine and aspartate aminotransferase enzymes. Moreover, animals with AFLD had increased levels of triacylglycerol in the serum and liver, likely due to reduced fatty acid metabolism caused by decreased PPAR-α expression, which is responsible for fatty acid oxidation, and increased expression of SREBP-1c, which is involved in fatty acid synthesis. With regard to inflammation, animals with AFLD exhibited elevated levels of pro-inflammatory cytokines, including TNF-a, IL-1β, and IL-6. The heightened oxidative stress, along with inflammation, led to an upregulation of cell death markers, such as caspase-3, and an increased Bax/Bcl-2 ratio. Overall, the findings of the review and meta-analysis indicate that ethanol metabolism reduces important markers of antioxidant defense while increasing inflammatory and apoptotic markers, thereby contributing to the development of AFLD.-
Formato: dc.formatapplication/pdf-
Idioma: dc.languageen-
Direitos: dc.rightsaberto-
Direitos: dc.rightsThis article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/). Fonte: PDF do artigo.-
Palavras-chave: dc.subjectAlcoholic steatosis-
Palavras-chave: dc.subjectAntioxidant enzymes-
Palavras-chave: dc.subjectLipid peroxidation-
Palavras-chave: dc.subjectApoptosis-
Palavras-chave: dc.subjectInflammation-
Título: dc.titleThe role of oxidative stress in alcoholic fatty liver disease : a systematic review and meta-analysis of preclinical studies.-
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