Mechanistic insights into curcumin’s role in modulating autophagy and redox imbalance in experimentally induced MASH

Background: Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by steatosis, inflammation, and fibrosis. Currently, no approved pharmacological treatment exists. Curcumin has shown potential therapeutic benefits, but its underlying mechanisms remain poorly understood.Aim: This...

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Bibliographic Details
Published in:Journal of Taibah University for Science Vol. 19; no. 1
Main Authors: Elkordy, Eman A., Zakaria, Soha S., AlHussaini, Khalid I., Sarhan, Naglaa I.
Format: Journal Article
Language:English
Published: Taylor & Francis Group 31.12.2025
Subjects:
apoptosis
Autophagy
curcumin
endoplasmic reticulum stress
metabolic dysfunction-associated steatohepatitis
oxidative stress
ISSN:1658-3655, 1658-3655
Online Access:Get full text
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Summary:Background: Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by steatosis, inflammation, and fibrosis. Currently, no approved pharmacological treatment exists. Curcumin has shown potential therapeutic benefits, but its underlying mechanisms remain poorly understood.Aim: This study evaluates curcumin’s role in ameliorating MASH in a high-fat diet (HFD)-induced rat model, focusing on endoplasmic reticulum (ER) stress, apoptosis, autophagy, and oxidative stress. Histological changes were also evaluated.Methods: Male rats were divided into control, MASH, and curcumin-treated MASH groups. Serum and hepatic biomarkers were analyzed including CCAAT/enhancer-binding protein homologous protein (CHOP), Bax, Bcl-2, and Beclin 1. Liver tissues were examined histologically.Results: Curcumin significantly downregulated protein kinase RNA-like endoplasmic reticulum kinase (PERK) and CHOP expression, restored Beclin-1 levels, reduced oxidative stress, and improved Bax/Bcl-2 ratios. Histological analysis confirmed reduced steatosis, and fibrosis.Conclusion: Curcumin alleviates MASH by modulating ER stress, oxidative stress, apoptosis, and autophagy, highlighting its therapeutic potential. Further clinical studies are needed.
ISSN:1658-3655
1658-3655
DOI:10.1080/16583655.2025.2467479