{"title":"Sodium Orthovanadate (SOV) mitigates alcohol & alcohol plus high-fat diet (HFD)-induced hepatotoxicity in rats.","authors":"Hema Rani, Anjana Devi, Navdeep Singh","doi":"10.14715/cmb/2025.71.8.5","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":520584,"journal":{"name":"Cellular and molecular biology (Noisy-le-Grand, France)","volume":"71 8","pages":"30-35"},"PeriodicalIF":0.0000,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cellular and molecular biology (Noisy-le-Grand, France)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14715/cmb/2025.71.8.5","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
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.