Protective role of vildagliptin against bisphenol-A induced liver injury: targeting oxidative stress, apoptosis, and endoplasmic reticulum stress.

IF 2.7 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2025-09-04 DOI:10.1080/13813455.2025.2555473

Naglaa Adly Abd Elazeem, Lamis Abdelghani Salamah, Marwa Abdeltawab Mohammed, Ghada Mahmoud Abd El Aziz, Shaimaa Abd El Tawab Fathi

{"title":"Protective role of vildagliptin against bisphenol-A induced liver injury: targeting oxidative stress, apoptosis, and endoplasmic reticulum stress.","authors":"Naglaa Adly Abd Elazeem, Lamis Abdelghani Salamah, Marwa Abdeltawab Mohammed, Ghada Mahmoud Abd El Aziz, Shaimaa Abd El Tawab Fathi","doi":"10.1080/13813455.2025.2555473","DOIUrl":null,"url":null,"abstract":"<p><p>Bisphenol-A (BPA) is an environmental pollutant that causes hepatic injury. The antioxidant activity of vildagliptin is confirmed. The present study investigated the protective effect of Vildagliptin against BPA-induced hepatotoxicity. Twenty four rats were divided randomly into 4 groups (6 rats/group): A control group, BPA group, BPA + Vildagliptin group and Vildagliptin group. All rats, except the controls were orally administered 30 mg/kg body weight BPA and/or 10 mg/kg Vildagliptin. AST, ALT, Triglycerides and albumin were measured in the serum. MDA, GPX, XBP1, Caspase 3 and BCL2 were measured in liver tissues. BPA group showed a significant decrease of albumin and GPX and a significant increase of triglycerides, AST, ALT and MDA. BPA caused up regulation of caspase3 and XBP1 while caused down regulation of BCL2. The co-administration of Vildagliptin reversed these hazards. The results of this study established the protective effect of Vildagliptin against BPA induced liver dysfunction.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-9"},"PeriodicalIF":2.7000,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archives of Physiology and Biochemistry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/13813455.2025.2555473","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}

引用次数: 0

Abstract

Bisphenol-A (BPA) is an environmental pollutant that causes hepatic injury. The antioxidant activity of vildagliptin is confirmed. The present study investigated the protective effect of Vildagliptin against BPA-induced hepatotoxicity. Twenty four rats were divided randomly into 4 groups (6 rats/group): A control group, BPA group, BPA + Vildagliptin group and Vildagliptin group. All rats, except the controls were orally administered 30 mg/kg body weight BPA and/or 10 mg/kg Vildagliptin. AST, ALT, Triglycerides and albumin were measured in the serum. MDA, GPX, XBP1, Caspase 3 and BCL2 were measured in liver tissues. BPA group showed a significant decrease of albumin and GPX and a significant increase of triglycerides, AST, ALT and MDA. BPA caused up regulation of caspase3 and XBP1 while caused down regulation of BCL2. The co-administration of Vildagliptin reversed these hazards. The results of this study established the protective effect of Vildagliptin against BPA induced liver dysfunction.

查看原文本刊更多论文

维格列汀对双酚a诱导的肝损伤的保护作用：针对氧化应激、细胞凋亡和内质网应激。

双酚a （BPA）是一种可引起肝脏损伤的环境污染物。证实了维格列汀的抗氧化活性。本研究探讨了维格列汀对双酚a肝毒性的保护作用。24只大鼠随机分为4组（6只/组）：对照组、BPA组、BPA +维格列汀组和维格列汀组。除对照组外，所有大鼠均口服30 mg/kg体重BPA和/或10 mg/kg维格列汀。测定血清中AST、ALT、甘油三酯、白蛋白含量。检测肝组织中MDA、GPX、XBP1、Caspase 3、BCL2的含量。BPA组白蛋白、GPX显著降低，甘油三酯、AST、ALT、MDA显著升高。BPA导致caspase3和XBP1上调，BCL2下调。维格列汀联合用药逆转了这些危害。本研究结果证实了维格列汀对双酚a诱导的肝功能障碍的保护作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.