水合吗啉能降低炎症介导的一氧化氮过量产生,并增强抗氧化机制,防止抗癌药物多柔比星对大鼠肝肾的氧化毒性。

IF 1.9 Q3 CHEMISTRY, MEDICINAL
Ademola C Famurewa, Chima A Ekeleme-Egedigwe, Patience N Ogbu, Ayodeji J Ajibare, Moshood A Folawiyo, Doris O Obasi, Arunaksharan Narayanankutty
{"title":"水合吗啉能降低炎症介导的一氧化氮过量产生,并增强抗氧化机制,防止抗癌药物多柔比星对大鼠肝肾的氧化毒性。","authors":"Ademola C Famurewa, Chima A Ekeleme-Egedigwe, Patience N Ogbu, Ayodeji J Ajibare, Moshood A Folawiyo, Doris O Obasi, Arunaksharan Narayanankutty","doi":"10.22038/AJP.2023.22392","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Doxorubicin (DOX) is a frontline antineoplastic drug that kills cancer cells through genotoxic mechanism; however, it induces organ toxicities. This study assayed whether morin hydrate (MOH) could abrogate DOX hepatorenal toxicity in rats.</p><p><strong>Materials and methods: </strong>There were 4 groups of rats: Control, MOH, DOX and MOH + DOX. Rats were administered MOH (orally, 100 mg/kg bw) for 7 consecutive days, while DOX was injected (40 mg/kg, ip) on the 5th day only. Hepatorenal function markers, and glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) activities were estimated in both organs. Hepatorenal glutathione (GSH), malondialdehyde (MDA), and nitric oxide (NO) levels were estimated with histopathology.</p><p><strong>Results: </strong>DOX significantly (p<0.05) reduced antioxidant enzyme activities and GSH level, while NO and MDA levels increased (p<0.05) compared to the control. DOX prominently altered hepatorenal indices and induced histopathological alterations. MOH abrogated the DOX hepatorenal toxicity and alleviated the histological lesions in the liver and kidney.</p><p><strong>Conclusion: </strong>MOH restored the indices via antioxidant mechanism and downregulation of NO overproduction in rats.</p>","PeriodicalId":8677,"journal":{"name":"Avicenna Journal of Phytomedicine","volume":null,"pages":null},"PeriodicalIF":1.9000,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10711573/pdf/","citationCount":"0","resultStr":"{\"title\":\"Morin hydrate downregulates inflammation-mediated nitric oxide overproduction and potentiates antioxidant mechanism against anticancer drug doxorubicin oxidative hepatorenal toxicity in rats.\",\"authors\":\"Ademola C Famurewa, Chima A Ekeleme-Egedigwe, Patience N Ogbu, Ayodeji J Ajibare, Moshood A Folawiyo, Doris O Obasi, Arunaksharan Narayanankutty\",\"doi\":\"10.22038/AJP.2023.22392\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>Doxorubicin (DOX) is a frontline antineoplastic drug that kills cancer cells through genotoxic mechanism; however, it induces organ toxicities. This study assayed whether morin hydrate (MOH) could abrogate DOX hepatorenal toxicity in rats.</p><p><strong>Materials and methods: </strong>There were 4 groups of rats: Control, MOH, DOX and MOH + DOX. Rats were administered MOH (orally, 100 mg/kg bw) for 7 consecutive days, while DOX was injected (40 mg/kg, ip) on the 5th day only. Hepatorenal function markers, and glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) activities were estimated in both organs. Hepatorenal glutathione (GSH), malondialdehyde (MDA), and nitric oxide (NO) levels were estimated with histopathology.</p><p><strong>Results: </strong>DOX significantly (p<0.05) reduced antioxidant enzyme activities and GSH level, while NO and MDA levels increased (p<0.05) compared to the control. DOX prominently altered hepatorenal indices and induced histopathological alterations. MOH abrogated the DOX hepatorenal toxicity and alleviated the histological lesions in the liver and kidney.</p><p><strong>Conclusion: </strong>MOH restored the indices via antioxidant mechanism and downregulation of NO overproduction in rats.</p>\",\"PeriodicalId\":8677,\"journal\":{\"name\":\"Avicenna Journal of Phytomedicine\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.9000,\"publicationDate\":\"2023-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10711573/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Avicenna Journal of Phytomedicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.22038/AJP.2023.22392\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CHEMISTRY, MEDICINAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Avicenna Journal of Phytomedicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.22038/AJP.2023.22392","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CHEMISTRY, MEDICINAL","Score":null,"Total":0}
引用次数: 0

摘要

目的:多柔比星(DOX)是通过基因毒性机制杀死癌细胞的一线抗肿瘤药物,但它也会引起器官毒性。本研究探讨了水合吗啉(MOH)能否减轻 DOX 对大鼠肝肾的毒性:材料和方法:大鼠共 4 组:对照组、MOH 组、DOX 组和 MOH + DOX 组。大鼠连续 7 天口服 MOH(100 毫克/千克体重),仅在第 5 天注射 DOX(40 毫克/千克,ip)。对两个器官的肝肾功能指标、谷胱甘肽过氧化物酶(GPx)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性进行了评估。通过组织病理学评估肝脏谷胱甘肽(GSH)、丙二醛(MDA)和一氧化氮(NO)的水平:结果:DOX明显(pMOH通过抗氧化机制和下调一氧化氮的过量产生,恢复了大鼠的各项指标。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Morin hydrate downregulates inflammation-mediated nitric oxide overproduction and potentiates antioxidant mechanism against anticancer drug doxorubicin oxidative hepatorenal toxicity in rats.

Objective: Doxorubicin (DOX) is a frontline antineoplastic drug that kills cancer cells through genotoxic mechanism; however, it induces organ toxicities. This study assayed whether morin hydrate (MOH) could abrogate DOX hepatorenal toxicity in rats.

Materials and methods: There were 4 groups of rats: Control, MOH, DOX and MOH + DOX. Rats were administered MOH (orally, 100 mg/kg bw) for 7 consecutive days, while DOX was injected (40 mg/kg, ip) on the 5th day only. Hepatorenal function markers, and glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) activities were estimated in both organs. Hepatorenal glutathione (GSH), malondialdehyde (MDA), and nitric oxide (NO) levels were estimated with histopathology.

Results: DOX significantly (p<0.05) reduced antioxidant enzyme activities and GSH level, while NO and MDA levels increased (p<0.05) compared to the control. DOX prominently altered hepatorenal indices and induced histopathological alterations. MOH abrogated the DOX hepatorenal toxicity and alleviated the histological lesions in the liver and kidney.

Conclusion: MOH restored the indices via antioxidant mechanism and downregulation of NO overproduction in rats.

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
Avicenna Journal of Phytomedicine
Avicenna Journal of Phytomedicine CHEMISTRY, MEDICINAL-
CiteScore
3.40
自引率
4.50%
发文量
17
审稿时长
6 weeks
×
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