{"title":"Pyridoxine exerts antioxidant effects on kidney injury manifestations in high-fat diet-induced obese rats","authors":"Onanong Jaruan , Sasivimon Promsan , Laongdao Thongnak , Nattavadee Pengrattanachot , Nichakorn Phengpol , Prempree Sutthasupha , Anusorn Lungkaphin","doi":"10.1016/j.cbi.2025.111513","DOIUrl":null,"url":null,"abstract":"<div><div>The modern diet contains a substantial level of fat which is believed to be one of the leading causes of the progression of kidney disease. Several studies have already demonstrated that consumption of a high-fat diet (HFD) induces inflammation and oxidative stress, causing activation of upstream mechanisms associated with kidney injury. For the prevention of such pathological events, a change in diet or the taking of nutritional supplements are recommended as alternative treatments. One of the forms of vitamin B6, pyridoxine (PN), has been shown to be an effective antioxidant and can also inhibit the formation of advanced-glycation end products (AGEs). In this study, the protective effects of PN (100 mg/kg/day for a period of eight weeks) against HFD-induced complications in obese rats were investigated. Rats fed on a HFD developed obesity which promoted inflammation, glucose intolerance, AGE receptor upregulation, oxidative stress, and kidney dysfunction. Intervention using PN mitigated obesity-related events and the impairment of kidney function by markedly reducing oxidative stress and also restoring the activity of antioxidant enzymes. Other studies have shown that some vitamin B6 derivatives inhibit the formation of AGEs but our study shows for the first time that PN exerted an antiglycative effect in this HFD-induced obesity model. Consequently, PN could potentially be a novel supplement for obese individuals to avoid kidney injury.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"415 ","pages":"Article 111513"},"PeriodicalIF":4.7000,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Chemico-Biological Interactions","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0009279725001437","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
The modern diet contains a substantial level of fat which is believed to be one of the leading causes of the progression of kidney disease. Several studies have already demonstrated that consumption of a high-fat diet (HFD) induces inflammation and oxidative stress, causing activation of upstream mechanisms associated with kidney injury. For the prevention of such pathological events, a change in diet or the taking of nutritional supplements are recommended as alternative treatments. One of the forms of vitamin B6, pyridoxine (PN), has been shown to be an effective antioxidant and can also inhibit the formation of advanced-glycation end products (AGEs). In this study, the protective effects of PN (100 mg/kg/day for a period of eight weeks) against HFD-induced complications in obese rats were investigated. Rats fed on a HFD developed obesity which promoted inflammation, glucose intolerance, AGE receptor upregulation, oxidative stress, and kidney dysfunction. Intervention using PN mitigated obesity-related events and the impairment of kidney function by markedly reducing oxidative stress and also restoring the activity of antioxidant enzymes. Other studies have shown that some vitamin B6 derivatives inhibit the formation of AGEs but our study shows for the first time that PN exerted an antiglycative effect in this HFD-induced obesity model. Consequently, PN could potentially be a novel supplement for obese individuals to avoid kidney injury.
期刊介绍:
Chemico-Biological Interactions publishes research reports and review articles that examine the molecular, cellular, and/or biochemical basis of toxicologically relevant outcomes. Special emphasis is placed on toxicological mechanisms associated with interactions between chemicals and biological systems. Outcomes may include all traditional endpoints caused by synthetic or naturally occurring chemicals, both in vivo and in vitro. Endpoints of interest include, but are not limited to carcinogenesis, mutagenesis, respiratory toxicology, neurotoxicology, reproductive and developmental toxicology, and immunotoxicology.