黄嘌呤衍生物对三氧化二砷诱导的小鼠肝脏和肾脏组织氧化应激的保护作用

IF 1.7 Q3 PHARMACOLOGY & PHARMACY
Drug Research Pub Date : 2024-03-01 Epub Date: 2024-02-13 DOI:10.1055/a-2247-5232
Navid Omidifar, Ahmad Gholami, Mansoureh Shokripour, Mohammad Ali Nourani, Milad Mohkam, Seyyed Mojtaba Mousavi, Seyyed Alireza Hashemi, Bagher Khorram, Amir Nili Ahmadabadi, Mahintaj Dara
{"title":"黄嘌呤衍生物对三氧化二砷诱导的小鼠肝脏和肾脏组织氧化应激的保护作用","authors":"Navid Omidifar, Ahmad Gholami, Mansoureh Shokripour, Mohammad Ali Nourani, Milad Mohkam, Seyyed Mojtaba Mousavi, Seyyed Alireza Hashemi, Bagher Khorram, Amir Nili Ahmadabadi, Mahintaj Dara","doi":"10.1055/a-2247-5232","DOIUrl":null,"url":null,"abstract":"<p><p>In this study, the protective efficacy of pentoxifylline (PTX) as a xanthine derivative against arsenic trioxide (ATO)-induced kidney and liver damage in mice was investigated. Thirty-six mice were divided into six groups, receiving intraperitoneal injections of saline, ATO, PTX, or a combination for four weeks. Blood samples were analyzed for serum biochemistry, while hepatic tissue underwent examination for histopathological changes and assessment of oxidative stress markers and antioxidant gene expression through Real-Time PCR. ATO exposure significantly increased serum markers (creatinine, ALT, BUN, ALP, AST) and induced histopathological changes in the liver. Moreover, it elevated renal and hepatic nitric oxide (NO) and lipid peroxidation (LPO) levels, and reduced antioxidant enzyme expression (CAT, GSR, GPx, MPO, SOD), total thiol groups (TTGs), and total antioxidant capacity (TAC). Conversely, PTX treatment effectively lowered serum hepatic and renal markers, improved antioxidant markers, and induced histopathological alterations. Notably, PTX did not significantly affect renal and hepatic NO levels. These findings suggest that PTX offers therapeutic potential in mitigating liver and acute kidney injuries induced by various insults, including exposure to ATO.</p>","PeriodicalId":11451,"journal":{"name":"Drug Research","volume":null,"pages":null},"PeriodicalIF":1.7000,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Protective Effects of Xanthine Derivatives Against Arsenic Trioxide-Induced Oxidative Stress in Mouse Hepatic and Renal Tissues.\",\"authors\":\"Navid Omidifar, Ahmad Gholami, Mansoureh Shokripour, Mohammad Ali Nourani, Milad Mohkam, Seyyed Mojtaba Mousavi, Seyyed Alireza Hashemi, Bagher Khorram, Amir Nili Ahmadabadi, Mahintaj Dara\",\"doi\":\"10.1055/a-2247-5232\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>In this study, the protective efficacy of pentoxifylline (PTX) as a xanthine derivative against arsenic trioxide (ATO)-induced kidney and liver damage in mice was investigated. Thirty-six mice were divided into six groups, receiving intraperitoneal injections of saline, ATO, PTX, or a combination for four weeks. Blood samples were analyzed for serum biochemistry, while hepatic tissue underwent examination for histopathological changes and assessment of oxidative stress markers and antioxidant gene expression through Real-Time PCR. ATO exposure significantly increased serum markers (creatinine, ALT, BUN, ALP, AST) and induced histopathological changes in the liver. Moreover, it elevated renal and hepatic nitric oxide (NO) and lipid peroxidation (LPO) levels, and reduced antioxidant enzyme expression (CAT, GSR, GPx, MPO, SOD), total thiol groups (TTGs), and total antioxidant capacity (TAC). Conversely, PTX treatment effectively lowered serum hepatic and renal markers, improved antioxidant markers, and induced histopathological alterations. Notably, PTX did not significantly affect renal and hepatic NO levels. These findings suggest that PTX offers therapeutic potential in mitigating liver and acute kidney injuries induced by various insults, including exposure to ATO.</p>\",\"PeriodicalId\":11451,\"journal\":{\"name\":\"Drug Research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.7000,\"publicationDate\":\"2024-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Drug Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1055/a-2247-5232\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/2/13 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"PHARMACOLOGY & PHARMACY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Drug Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1055/a-2247-5232","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/2/13 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}
引用次数: 0

摘要

本研究探讨了作为黄嘌呤衍生物的喷托塞林(PTX)对三氧化二砷(ATO)诱导的小鼠肝肾损伤的保护作用。研究人员将 36 只小鼠分为 6 组,分别腹腔注射生理盐水、ATO、PTX 或其组合,为期四周。对血样进行血清生化分析,同时对肝组织进行组织病理学变化检查,并通过实时 PCR 评估氧化应激标记物和抗氧化基因的表达。暴露于 ATO 会明显增加血清指标(肌酐、谷丙转氨酶、尿素氮、谷草转氨酶、谷草转氨酶),并诱发肝脏组织病理学变化。此外,它还会升高肾脏和肝脏的一氧化氮(NO)和脂质过氧化(LPO)水平,降低抗氧化酶(CAT、GSR、GPx、MPO、SOD)、总硫醇基团(TTGs)和总抗氧化能力(TAC)的表达。相反,PTX 治疗可有效降低血清肝脏和肾脏指标,改善抗氧化指标,并诱导组织病理学改变。值得注意的是,PTX 对肾脏和肝脏的 NO 水平没有明显影响。这些研究结果表明,PTX 在减轻各种损伤(包括暴露于 ATO)引起的肝脏和急性肾脏损伤方面具有治疗潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Protective Effects of Xanthine Derivatives Against Arsenic Trioxide-Induced Oxidative Stress in Mouse Hepatic and Renal Tissues.

In this study, the protective efficacy of pentoxifylline (PTX) as a xanthine derivative against arsenic trioxide (ATO)-induced kidney and liver damage in mice was investigated. Thirty-six mice were divided into six groups, receiving intraperitoneal injections of saline, ATO, PTX, or a combination for four weeks. Blood samples were analyzed for serum biochemistry, while hepatic tissue underwent examination for histopathological changes and assessment of oxidative stress markers and antioxidant gene expression through Real-Time PCR. ATO exposure significantly increased serum markers (creatinine, ALT, BUN, ALP, AST) and induced histopathological changes in the liver. Moreover, it elevated renal and hepatic nitric oxide (NO) and lipid peroxidation (LPO) levels, and reduced antioxidant enzyme expression (CAT, GSR, GPx, MPO, SOD), total thiol groups (TTGs), and total antioxidant capacity (TAC). Conversely, PTX treatment effectively lowered serum hepatic and renal markers, improved antioxidant markers, and induced histopathological alterations. Notably, PTX did not significantly affect renal and hepatic NO levels. These findings suggest that PTX offers therapeutic potential in mitigating liver and acute kidney injuries induced by various insults, including exposure to ATO.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Drug Research
Drug Research PHARMACOLOGY & PHARMACY-
CiteScore
3.50
自引率
0.00%
发文量
67
期刊介绍: Drug Research (formerly Arzneimittelforschung) is an international peer-reviewed journal with expedited processing times presenting the very latest research results related to novel and established drug molecules and the evaluation of new drug development. A key focus of the publication is translational medicine and the application of biological discoveries in the development of drugs for use in the clinical environment. Articles and experimental data from across the field of drug research address not only the issue of drug discovery, but also the mathematical and statistical methods for evaluating results from industrial investigations and clinical trials. Publishing twelve times a year, Drug Research includes original research articles as well as reviews, commentaries and short communications in the following areas: analytics applied to clinical trials chemistry and biochemistry clinical and experimental pharmacology drug interactions efficacy testing pharmacodynamics pharmacokinetics teratology toxicology.
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信