Evidence map›Paper›PMID 39172304›Full record

ArticleMolecular biology reports2024

Exercise-activated hepatic autophagy combined with silymarin is associated with suppression of apoptosis in rats subjected to dexamethasone induced- fatty liver damage.

Fatemeh Mokhtari Andani, Elahe Talebi-Garakani, Ghorbangol Ashabi, Mahtab Ganbarirad, Mohammad Hashemnia, Mohammadreza Sharifi, Maedeh Ghasemi

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Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Fatemeh Mokhtari AndaniDepartment of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Elahe Talebi-GarakaniDepartment of Exercise Physiology, Faculty of Sports Sciences, University of Mazandaran, Mazandaran, Iran.ORCID https://orcid.org/0000-0001-7499-8852
Ghorbangol AshabiDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0002-4853-092X
Mahtab GanbariradGerash Cellular and Molecular Research Center, Gerash University of Medical Sciences, Gerash, Iran.
Mohammad HashemniaDepartment of Pathobiology, Faculty of Veterinary Medicine, Razi University, Kermanshah, Iran.
Mohammadreza SharifiDepartment of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.ORCID https://orcid.org/0000-0002-1538-9034
Maedeh GhasemiDepartment of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. ghasemi.m@med.mui.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimThere is a need for effective treatments for non-alcoholic fatty liver disease (NAFLD) that are economically inexpensive, and have few side effects. The present study aimed to investigate exercise training and silymarin on hepatocyte death factors in rats with liver damage.

methodsForty-nine male Wistar rats were assigned to seven groups: sedentary control, fatty liver control (DEX), fatty liver + high-intensity interval training (HIIT), fatty liver + HIIT + silymarin (HIIT + SILY), fatty liver + continuous training (CT), fatty liver + CT + silymarin (CT + SILY), and fatty liver + silymarin (SILY). A subcutaneous injection of dexamethasone for 7 days was used to induce fatty liver in rats. Masson's trichrome and hematoxylin-eosin staining were done to evaluate hepatic injury. The hepatocyte apoptosis was determined by TUNEL assay. Real-Time PCR was conducted to evaluate the gene expressions of caspase-9, adenosine monophosphate-activated protein kinase (AMPKα1), mitofusin 2 (Mfn2), and damage-regulated autophagy modulator (DRAM). Liver tissue changes and serum levels of liver enzymes were also evaluated.

resultsLiver apoptosis was decreased in the CT, HIIT, HIIT + SILY and CT + SILY groups compared to the DEX group. Both continuous and high-intensity training models produced beneficial alterations in liver morphology and hepatic injuries that were significant in exercise training + silymarin group. This impact was accompanied by increased AMPKα1 and DRAM gene expression and decreased caspase-9 and Mfn2 gene expression. Liver enzyme levels were high in the DEX group and treatment with silymarin significantly reduced it.

conclusionSilymarin supplementation combined with interval or continuous training substantially improves DEX-induced hepatic steatosis and hepatocyte injury mostly through suppressing liver apoptosis and upregulating autophagy, which may provide a novel perspective for NAFLD treatment.

Indexed as

ApoptosisAutophagyDexamethasoneLiverNon-alcoholic Fatty Liver DiseasePhysical Conditioning, AnimalRats, WistarSilymarinAMP-Activated Protein KinasesAnimalsCaspase 9Disease Models, AnimalGTP PhosphohydrolasesHepatocytesMaleMitochondrial ProteinsAMP-Activated Protein KinasesCaspase 9DexamethasoneGTP PhosphohydrolasesMfn2 protein, ratMitochondrial ProteinsPrkaa1 protein, ratSilymarinApoptosisAutophagyContinuous trainingDexamethasoneHIITNAFLDSilymarin

Identifiers

PMID39172304

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.