Orlistat and metformin combination ameliorates obesity-induced renal injury via suppressing renal oxidative stress in male rats.

IF 2.2 4区 医学 Q3 TOXICOLOGY Toxicology Research Pub Date : 2024-08-21 eCollection Date: 2024-08-01 DOI:10.1093/toxres/tfae135
Khadeejah Alsolami, Reham Z Hamza
{"title":"Orlistat and metformin combination ameliorates obesity-induced renal injury via suppressing renal oxidative stress in male rats.","authors":"Khadeejah Alsolami, Reham Z Hamza","doi":"10.1093/toxres/tfae135","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Orlistat (ORS) and metformin (MEF) are robustly used as well-established clinical drugs for the treatment for both obesity and the consequences of diabetes mellitus. Additionally, no study has been conducted to explore the consequence of the combination of both ORS and MEF on the kidneys of rats with obesity-induced renal injury (OBS).</p><p><strong>Objectives: </strong>Therefore, the objective of the current research was designed to explore the possible ameliorative effects of either ORS and/or MEF or their combination against obesity (OBS) induced experimental renal oxidative stress.</p><p><strong>Methods: </strong>Renal oxidative stress was investigated at redox histopathological and immunohistological points in the kidney tissues.</p><p><strong>Results: </strong>The levels of urea, uric acid, and creatinine increased with the obesity effect; in addition, the myeloperoxidase (MPO) and xanthine oxidase (XO) activators were elevated significantly with the induction of OBS. The levels of non-enzymatic antioxidants (glutathione and thiol) declined sharply in OBS rats as compared to the normal group.</p><p><strong>Conclusion: </strong>The data displayed that the combination of both ORS and MEF declined the obesity effects significantly by reducing the level of peroxidation (MDA), and enhancement intracellular antioxidant enzymes. These biochemical findings were supported by histopathology, immunohistochemistry, and Masson-Trichrome evaluation, which showed minor morphological changes in the kidneys of rats.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":null,"pages":null},"PeriodicalIF":2.2000,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11336066/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/toxres/tfae135","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/8/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"TOXICOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Orlistat (ORS) and metformin (MEF) are robustly used as well-established clinical drugs for the treatment for both obesity and the consequences of diabetes mellitus. Additionally, no study has been conducted to explore the consequence of the combination of both ORS and MEF on the kidneys of rats with obesity-induced renal injury (OBS).

Objectives: Therefore, the objective of the current research was designed to explore the possible ameliorative effects of either ORS and/or MEF or their combination against obesity (OBS) induced experimental renal oxidative stress.

Methods: Renal oxidative stress was investigated at redox histopathological and immunohistological points in the kidney tissues.

Results: The levels of urea, uric acid, and creatinine increased with the obesity effect; in addition, the myeloperoxidase (MPO) and xanthine oxidase (XO) activators were elevated significantly with the induction of OBS. The levels of non-enzymatic antioxidants (glutathione and thiol) declined sharply in OBS rats as compared to the normal group.

Conclusion: The data displayed that the combination of both ORS and MEF declined the obesity effects significantly by reducing the level of peroxidation (MDA), and enhancement intracellular antioxidant enzymes. These biochemical findings were supported by histopathology, immunohistochemistry, and Masson-Trichrome evaluation, which showed minor morphological changes in the kidneys of rats.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
奥利司他和二甲双胍复方制剂通过抑制雄性大鼠肾脏氧化应激改善肥胖引起的肾损伤
背景:奥利司他(ORS)和二甲双胍(MEF)是治疗肥胖症和糖尿病后遗症的有效临床药物。此外,目前还没有研究探讨 ORS 和二甲双胍联合使用对肥胖诱发肾损伤(OBS)大鼠肾脏的影响:因此,本研究旨在探讨 ORS 和/或 MEF 或它们的组合对肥胖(OBS)诱导的实验性肾氧化应激可能产生的改善作用:方法:从肾脏组织的氧化还原组织病理学和免疫组织学角度对肾脏氧化应激进行研究:结果:尿素、尿酸和肌酐的水平随肥胖效应而升高;此外,髓过氧化物酶(MPO)和黄嘌呤氧化酶(XO)的活化因子随OBS的诱导而显著升高。与正常组相比,OBS 大鼠的非酶抗氧化剂(谷胱甘肽和硫醇)水平急剧下降:数据显示,ORS 和 MEF 的组合能降低过氧化物(MDA)的水平,增强细胞内抗氧化酶的作用,从而显著减轻肥胖症的影响。组织病理学、免疫组化和马森-特里克罗米评估结果表明,大鼠肾脏的形态发生了轻微变化,这为上述生化研究结果提供了佐证。
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 去求助
来源期刊
Toxicology Research
Toxicology Research TOXICOLOGY-
CiteScore
3.60
自引率
0.00%
发文量
82
期刊介绍: A multi-disciplinary journal covering the best research in both fundamental and applied aspects of toxicology
期刊最新文献
Brain mitochondrial damage attenuation by quercetin and N-acetyl cysteine: peripheral and central antiemetic effects. Effect of baicalin and baicalin-bovine serum albumin nanoparticle against bendiocarb exposure in rats. Maternal exposure to Di-n-butyl phthalate (DBP) inhibit orexin receptor 1 (OX1R) expression to prevent Sertoli cells proliferation through the AKT signaling pathway. Boosting impacts of Acacia nilotica against hepatic toxicity induced by gentamicin: biochemical, anti-inflammatory and immunohistochemical study. Mechanistic insights into Retama raetam's anti-proliferative and pro-apoptotic effects in A549 lung cancer cells: targeting PI3K/Akt pathway and ROS production.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1