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Copyright (c) 2025 Hema Rani, Anjana Devi, Navdeep Singh
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Sodium Orthovanadate (SOV) mitigates alcohol & alcohol plus high-fat diet (HFD)-induced hepatotoxicity in rats
Corresponding Author(s) : Hema Rani
Cellular and Molecular Biology,
Vol. 71 No. 8: Issue 8
Abstract
Alcoholic fatty liver disease (AFLD) is a leading cause of chronic liver disease worldwide, contributing to significant morbidity and mortality. Despite its growing prevalence, no FDA-approved pharmacological treatments exist, leaving lifestyle modifications as the primary intervention. AFLD pathogenesis involves a complex interplay of lipid accumulation, oxidative stress, insulin resistance, and inflammation, highlighting the need for innovative therapeutic approaches. However, sodium orthovanadate (SOV), an inorganic vanadium-based compound, is a potent inhibitor of protein tyrosine phosphatases (PTPs), including PTP1B—a key regulator of insulin signalling and metabolic homeostasis. SOV has demonstrated insulin-mimetic properties and has shown promise in preclinical models of metabolic disorders. Given the emerging role of PTP1B in hepatic insulin resistance and lipid dysregulation, we hypothesize that SOV may offer therapeutic benefits in AFLD by modulating biochemical parameters and oxidative stress in liver. In this study, we investigate the effects of SOV in two rodent models of AFLD: (1) alcohol-induced liver disease and (2) high-fat diet plus alcohol-induced liver disease. We assess Biochemical Parameters like alkaline Phosphatase (ALP), aspartate amino transferase (AST), alanine amino transferase (ALT), lactate dehydrogenase (LDH), total bilirubin, cholesterol, uric acid, triglyceride. Tissue analysis like TBARS/MDA activity, Glutathione (reduced GSH) assay, Glutathione peroxidase (GPx) activity, Superoxide Dismutase, Catalase activity, and Histopathology to determine whether SOV can mitigate AFLD progression. Our research shows that SOV has promise as a treatment for fatty liver disease brought on by alcohol. Improvements in oxidative stress control,biochemical markers most likely mediate its hepatoprotective benefits. By uncovering the therapeutic potential of SOV, this study may pave the way for novel pharmacological strategies to combat fatty liver diseases.
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