Luana Cristina Faria Carvalho, Flávia Monteiro Ferreira, Bruna Vidal Dias, Daniela Couto de Azevedo, Gustavo Henrique Bianco de Souza, Matheus Marque Milagre, Marta de Lana, Paula Melo de Abreu Vieira, Cláudia Martins Carneiro, Sílvia de Paula-Gomes, Silvia Dantas Cangussu, Daniela Caldeira Costa
{"title":"Silymarin inhibits the lipogenic pathway and reduces worsening of non-alcoholic fatty liver disease (NAFLD) in mice.","authors":"Luana Cristina Faria Carvalho, Flávia Monteiro Ferreira, Bruna Vidal Dias, Daniela Couto de Azevedo, Gustavo Henrique Bianco de Souza, Matheus Marque Milagre, Marta de Lana, Paula Melo de Abreu Vieira, Cláudia Martins Carneiro, Sílvia de Paula-Gomes, Silvia Dantas Cangussu, Daniela Caldeira Costa","doi":"10.1080/13813455.2022.2138445","DOIUrl":null,"url":null,"abstract":"<p><strong>Context: </strong>The role of silymarin in hepatic lipid dysfunction and its possible mechanisms of action were investigated.</p><p><strong>Objective: </strong>To evaluate the effects of silymarin on hepatic and metabolic profiles in mice fed with 30% fructose for 8 weeks.</p><p><strong>Methods: </strong>We evaluated the antioxidant profile of silymarin; mice consumed 30% fructose and were treated with silymarin (120<b> </b>mg/kg/day or 240 mg/kg/day). We performed biochemical, redox status, and histopathological assays. RT-qPCR was performed to detect ACC-1, ACC-2, FAS, and CS expression, and western blotting to detect PGC-1α levels.</p><p><strong>Results: </strong>Silymarin contains high levels of phenolic compounds and flavonoids and exhibited significant antioxidant capacity <i>in vitro. In vivo</i>, the fructose-fed groups showed increased levels of AST, ALT, SOD/CAT, TBARS, hepatic TG, and cholesterol, as well as hypertriglyceridaemia, hypercholesterolaemia, and increased ACC-1 and FAS. Silymarin treatment reduced these parameters and increased mRNA levels and activity of hepatic citrate synthase.</p><p><strong>Conclusions: </strong>These results suggest that silymarin reduces worsening of NAFLD.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":2.5000,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archives of Physiology and Biochemistry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/13813455.2022.2138445","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/11/3 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 0
Abstract
Context: The role of silymarin in hepatic lipid dysfunction and its possible mechanisms of action were investigated.
Objective: To evaluate the effects of silymarin on hepatic and metabolic profiles in mice fed with 30% fructose for 8 weeks.
Methods: We evaluated the antioxidant profile of silymarin; mice consumed 30% fructose and were treated with silymarin (120mg/kg/day or 240 mg/kg/day). We performed biochemical, redox status, and histopathological assays. RT-qPCR was performed to detect ACC-1, ACC-2, FAS, and CS expression, and western blotting to detect PGC-1α levels.
Results: Silymarin contains high levels of phenolic compounds and flavonoids and exhibited significant antioxidant capacity in vitro. In vivo, the fructose-fed groups showed increased levels of AST, ALT, SOD/CAT, TBARS, hepatic TG, and cholesterol, as well as hypertriglyceridaemia, hypercholesterolaemia, and increased ACC-1 and FAS. Silymarin treatment reduced these parameters and increased mRNA levels and activity of hepatic citrate synthase.
Conclusions: These results suggest that silymarin reduces worsening of NAFLD.
期刊介绍:
Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders.
The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications.
Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics:
-Dysregulation of hormone receptors and signal transduction
-Contribution of gene variants and gene regulatory processes
-Impairment of intermediary metabolism at the cellular level
-Secretion and metabolism of peptides and other factors that mediate cellular crosstalk
-Therapeutic strategies for managing metabolic diseases
Special issues dedicated to topics in the field will be published regularly.