文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期，新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2025

芒果苷对甲氨蝶呤诱导的雄性大鼠肾损伤的肾保护作用：过氧化物酶体增殖物激活受体γ介导的抗氧化活性

Reno-protective effect of mangiferin against methotrexate-induced kidney damage in male rats: PPARγ-mediated antioxidant activity.

作者信息

Attia Seba Hassan, Elshazly Shimaa Mustafa, Abdelaal Mahmoud Mohamed, Soliman Eman

机构信息

Clinical Pharmacology Department, Faculty of Medicine, Zagazig University, Egypt.

Pharmacology and Toxicology Department, Faculty of Pharmacy, Zagazig University, Egypt.

出版信息

Saudi Pharm J. 2022 Sep;30(9):1252-1261. doi: 10.1016/j.jsps.2022.06.026. Epub 2022 Jul 1.

DOI:10.1016/j.jsps.2022.06.026
PMID:36249937
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9561181/
Abstract

Methotrexate (MTX) is an immunosuppressant used for the treatment of cancer and autoimmune diseases. MTX has a major adverse effect, acute kidney injury, which limits its use. Mangiferin (MF) is a natural bioactive xanthonoid used as a traditional herbal supplement to boost the immune system due to its potent anti-inflammatory and antioxidant activity. The present study evaluates the protective effect of MF against MTX-induced kidney damage. Male Wistar rats received MTX to induce nephrotoxicity or were pretreated with MF for 10 constitutive days before MTX administration. MF dose-dependently improved renal functions of MTX-treated rats and this activity was correlated with increased renal expression of PPARγ, a well-known transcriptional regulator of the immune response. Pretreating rats with PPARγ inhibitor, BADGE, reduced the reno-protective activity of MF. Furthermore, MF treatment significantly reduced MTX-induced upregulation of the pro-inflammatory (NFκB, interleukin-1ß, TNF-α, and COX-2), oxidative stress (Nrf-2, hemoxygenase-1, glutathione, and malondialdehyde), and nitrosative stress (nitric oxide and iNOS) markers in the kidney. Importantly, BADGE treatment significantly reduced the anti-inflammatory and antioxidant activity of MF. Therefore, our data suggest that the reno-protective effect of MF against MTX-induced nephrotoxicity is due to inhibition of inflammation and oxidative stress in a PPAR-γ-dependent manner.

摘要

甲氨蝶呤（MTX）是一种用于治疗癌症和自身免疫性疾病的免疫抑制剂。MTX有一个主要的不良反应，即急性肾损伤，这限制了它的使用。芒果苷（MF）是一种天然的生物活性呫吨酮，由于其强大的抗炎和抗氧化活性，被用作传统的草药补充剂来增强免疫系统。本研究评估了MF对MTX诱导的肾损伤的保护作用。雄性Wistar大鼠接受MTX以诱导肾毒性，或者在给予MTX前连续10天用MF进行预处理。MF剂量依赖性地改善了MTX处理大鼠的肾功能，并且这种活性与肾脏中PPARγ（一种众所周知的免疫反应转录调节因子）表达的增加相关。用PPARγ抑制剂BADGE预处理大鼠降低了MF的肾保护活性。此外，MF治疗显著降低了MTX诱导的肾脏中促炎（NFκB、白细胞介素-1β、肿瘤坏死因子-α和环氧化酶-2）、氧化应激（Nrf-2、血红素加氧酶-1、谷胱甘肽和丙二醛）以及亚硝化应激（一氧化氮和诱导型一氧化氮合酶）标志物的上调。重要的是，BADGE治疗显著降低了MF抗炎和抗氧化活性。因此，我们的数据表明MF对MTX诱导的肾毒性的肾保护作用是由于以PPAR-γ依赖性方式抑制炎症和氧化应激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/2310d3e22928/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/823a2928c068/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/10e5b0676bb2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/35a51b2f8661/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/e44a0cc605e5/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/57698c170ba4/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/1e8dd4fb4a13/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/597cc73e5fa6/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/d3233b4ab831/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/2310d3e22928/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/823a2928c068/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/10e5b0676bb2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/35a51b2f8661/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/e44a0cc605e5/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/57698c170ba4/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/1e8dd4fb4a13/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/597cc73e5fa6/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/d3233b4ab831/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48d4/9561181/2310d3e22928/gr8.jpg

相似文献

[1]
Reno-protective effect of mangiferin against methotrexate-induced kidney damage in male rats: PPARγ-mediated antioxidant activity.

Saudi Pharm J. 2022-9

[2]
Platelet Rich Plasma and Adipose-Derived Mesenchymal Stem Cells Mitigate Methotrexate-Induced Nephrotoxicity in Rat via Nrf2/Pparγ/HO-1 and NF-Κb/Keap1/Caspase-3 Signaling Pathways: Oxidative Stress and Apoptosis Interplay.

Toxics. 2023-4-22

[3]
Protective effect of peroxisome proliferator activator receptor (PPAR)-α and -γ ligands against methotrexate-induced nephrotoxicity.

Immunopharmacol Immunotoxicol. 2014-2-13

[4]
Methotrexate hepatotoxicity is associated with oxidative stress, and down-regulation of PPARγ and Nrf2: Protective effect of 18β-Glycyrrhetinic acid.

Chem Biol Interact. 2017-4-13

[5]
Quillaja saponin mitigates methotrexate-provoked renal injury; insight into Nrf-2/Keap-1 pathway modulation with suppression of oxidative stress and inflammation.

J Pharm Health Care Sci. 2024-4-9

[6]
Antioxidant and anti-inflammatory effects of virgin coconut oil supplementation abrogate acute chemotherapy oxidative nephrotoxicity induced by anticancer drug methotrexate in rats.

Biomed Pharmacother. 2017-12-7

[7]
Potential protective effect of etanercept and aminoguanidine in methotrexate-induced hepatotoxicity and nephrotoxicity in rats.

Eur J Pharmacol. 2015-8-30

[8]
Ferulic acid protects against methotrexate nephrotoxicity via activation of Nrf2/ARE/HO-1 signaling and PPARγ, and suppression of NF-κB/NLRP3 inflammasome axis.

Food Funct. 2019-7-10

[9]
Protective Mechanisms of Thymoquinone on Methotrexate-induced Intestinal Toxicity in Rats.

Pharmacogn Mag. 2016-1

[10]
Berberine ameliorates methotrexate-induced liver injury by activating Nrf2/HO-1 pathway and PPARγ, and suppressing oxidative stress and apoptosis in rats.

Biomed Pharmacother. 2017-7-29

引用本文的文献

[1]
Quillaja saponin mitigates methotrexate-provoked renal injury; insight into Nrf-2/Keap-1 pathway modulation with suppression of oxidative stress and inflammation.

J Pharm Health Care Sci. 2024-4-9

[2]
Possible Implication of Nrf2, PPAR-γ and MAPKs Signaling in the Protective Role of Mangiferin against Renal Ischemia/Reperfusion in Rats.

Pharmaceuticals (Basel). 2022-12-21

本文引用的文献

[1]
Geraniol Averts Methotrexate-Induced Acute Kidney Injury via Keap1/Nrf2/HO-1 and MAPK/NF-κB Pathways.

Curr Issues Mol Biol. 2021-10-24

[2]
PPARγ and TGFβ-Major Regulators of Metabolism, Inflammation, and Fibrosis in the Lungs and Kidneys.

Int J Mol Sci. 2021-9-28

[3]
Anticancer and anti-inflammatory properties of mangiferin: A review of its molecular mechanisms.

Food Chem Toxicol. 2021-3

[4]
NRF2, a Transcription Factor for Stress Response and Beyond.

Int J Mol Sci. 2020-7-6

[5]
PPAR and Its Agonists in Chronic Kidney Disease.

Int J Nephrol. 2020-2-25

[6]
Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion.

Front Pharmacol. 2020-2-7

[7]
Mangiferin Alleviates Renal Interstitial Fibrosis in Streptozotocin-Induced Diabetic Mice through Regulating the PTEN/PI3K/Akt Signaling Pathway.

J Diabetes Res. 2020-1-31

[8]
PPAR-γ agonist, pioglitazone, reduced oxidative and endoplasmic reticulum stress associated with L-NAME-induced hypertension in rats.

Life Sci. 2019-11-12

[9]
Ferulic acid protects against methotrexate nephrotoxicity via activation of Nrf2/ARE/HO-1 signaling and PPARγ, and suppression of NF-κB/NLRP3 inflammasome axis.

Food Funct. 2019-7-10

[10]
PPAR gamma agonist, pioglitazone, rescues liver damage induced by renal ischemia/reperfusion injury.

Toxicol Appl Pharmacol. 2018-10-26

文献AI研究员

20分钟写一篇综述，助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

推荐工具

医学文档翻译智能文献检索