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Melatonin Prevents Thioacetamide-Induced Gut Leakiness and Liver Fibrosis Through the Gut-Liver Axis via Modulating Sirt1-Related Deacetylation of Gut Junctional Complex and Hepatic Proteins.
Rungratanawanich, Wiramon; LeFort, Karli Rae; Cho, Young-Eun; Li, Xiaoling; Song, Byoung-Joon.
Afiliación
  • Rungratanawanich W; Section of Molecular Pharmacology and Toxicology, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland, USA.
  • LeFort KR; Section of Molecular Pharmacology and Toxicology, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland, USA.
  • Cho YE; Department of Food and Nutrition, Andong National University, Andong, Republic of Korea.
  • Li X; Signal Transduction Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
  • Song BJ; Section of Molecular Pharmacology and Toxicology, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland, USA.
J Pineal Res ; 76(6): e13007, 2024 Sep.
Article en En | MEDLINE | ID: mdl-39269018
ABSTRACT
Intestinal barrier dysfunction with high serum endotoxin is common in patients with liver fibrosis, but the mechanisms underlying liver fibrosis remain unclear. Melatonin is a well-recognized antioxidant and an anti-inflammatory agent that benefits multiple organs. However, the beneficial effects of melatonin on gut leakiness-associated liver fibrosis have not been systemically studied. Here, we investigated the protective mechanisms of melatonin against thioacetamide (TAA)-induced gut barrier dysfunction and hepatic fibrosis by focusing on posttranslational protein modifications through the gut-liver axis. Our results showed that gut leakiness markers, including decreased gut tight/adherens junction proteins (TJ/AJs) with increased intestinal deformation, apoptosis, and serum endotoxin, were observed early at 1 week after TAA exposure. Liver injury, apoptosis, and fibrosis were prominent at 2 and 4 weeks. Mechanistically, we found that gut TJ/AJs were hyper-acetylated, followed by ubiquitin-dependent proteolysis, leading to their degradation and gut leakiness. Gut dysbiosis, hepatic protein hyper-acetylation, and SIRT1 downregulation were also observed. Consistently, intestinal Sirt1 deficiency greatly enhanced protein hyper-acetylation, gut leakiness, endotoxemia, and liver fibrosis. Pretreatment with melatonin prevented or improved all these changes in both the gut and liver. Furthermore, melatonin blunted protein acetylation and injury in TAA-exposed T84 human intestinal and AML12 mouse liver cells. Overall, this study demonstrated novel mechanisms by which melatonin prevents gut leakiness and liver fibrosis through the gut-liver axis by attenuating the acetylation of intestinal and hepatic proteins. Thus, melatonin consumption can become a potentially safe supplement for liver fibrosis patients by preventing protein hyper-acetylation and gut leakiness.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Tioacetamida / Sirtuina 1 / Cirrosis Hepática / Melatonina Límite: Animals / Humans / Male Idioma: En Revista: J Pineal Res Asunto de la revista: ENDOCRINOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Tioacetamida / Sirtuina 1 / Cirrosis Hepática / Melatonina Límite: Animals / Humans / Male Idioma: En Revista: J Pineal Res Asunto de la revista: ENDOCRINOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido