{"title":"Cadmium-Induced Kidney Apoptosis Based on the IRE1α-XBP1 Signaling Pathway and the Protective Effect of Quercetin.","authors":"Liuxin Wang, Weiwei Cao, Ting Wu","doi":"10.3390/toxics13020129","DOIUrl":null,"url":null,"abstract":"<p><p>Cadmium (Cd) is an important environmental pollutant that can enter the body and inflict kidney damage. Quercetin (Que) is a natural flavonoid compound that can alleviate kidney damage in Cd-treated rats, but the specific mechanism is unclear. Herein, 24 male Sprague-Dawley rats were divided into four groups, namely the control, Cd, Cd + Que, and Que groups. Four weeks later, the rats were anesthetized with ether and were euthanized; then, their blood was collected and their kidneys were removed. Renal function markers were measured. Kidney tissue structure was observed by HE staining, cell apoptosis was detected by the TUNEL method, and mRNA and protein expression levels in the IRE1α-XBP1 apoptosis signaling pathway were analyzed by RT-PCR and Western blotting. Results showed that the Cd treatment group exhibited decreased renal dysfunction and pathologic injury. Cd-induced tissue damage and cell apoptosis and significantly increased the mRNA and protein expression levels (<i>p</i> < 0.01) related to the IRE1α-XBP1 signaling pathway. Compared with the Cd group, the Cd + Que group exhibited increased renal dysfunction. Conversely, kidney tissue damage and renal cell apoptosis decreased, and the mRNA and protein expression levels of IRE1α and XBP1 significantly decreased (<i>p</i> < 0.01). Cd treatment inflicted renal damage. Therefore, Que can restore the kidney tissue damage and alleviate the cell apoptosis caused by Cd through the inhibition of the IRE1α-XBP1 signaling pathway.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"13 2","pages":""},"PeriodicalIF":3.9000,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxics","FirstCategoryId":"93","ListUrlMain":"https://doi.org/10.3390/toxics13020129","RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Cadmium (Cd) is an important environmental pollutant that can enter the body and inflict kidney damage. Quercetin (Que) is a natural flavonoid compound that can alleviate kidney damage in Cd-treated rats, but the specific mechanism is unclear. Herein, 24 male Sprague-Dawley rats were divided into four groups, namely the control, Cd, Cd + Que, and Que groups. Four weeks later, the rats were anesthetized with ether and were euthanized; then, their blood was collected and their kidneys were removed. Renal function markers were measured. Kidney tissue structure was observed by HE staining, cell apoptosis was detected by the TUNEL method, and mRNA and protein expression levels in the IRE1α-XBP1 apoptosis signaling pathway were analyzed by RT-PCR and Western blotting. Results showed that the Cd treatment group exhibited decreased renal dysfunction and pathologic injury. Cd-induced tissue damage and cell apoptosis and significantly increased the mRNA and protein expression levels (p < 0.01) related to the IRE1α-XBP1 signaling pathway. Compared with the Cd group, the Cd + Que group exhibited increased renal dysfunction. Conversely, kidney tissue damage and renal cell apoptosis decreased, and the mRNA and protein expression levels of IRE1α and XBP1 significantly decreased (p < 0.01). Cd treatment inflicted renal damage. Therefore, Que can restore the kidney tissue damage and alleviate the cell apoptosis caused by Cd through the inhibition of the IRE1α-XBP1 signaling pathway.
ToxicsChemical Engineering-Chemical Health and Safety
CiteScore
4.50
自引率
10.90%
发文量
681
审稿时长
6 weeks
期刊介绍:
Toxics (ISSN 2305-6304) is an international, peer-reviewed, open access journal which provides an advanced forum for studies related to all aspects of toxic chemicals and materials. It publishes reviews, regular research papers, and short communications. Our aim is to encourage scientists to publish their experimental and theoretical results in detail. There is, therefore, no restriction on the maximum length of the papers, although authors should write their papers in a clear and concise way. The full experimental details must be provided so that the results can be reproduced. Electronic files or software regarding the full details of calculations and experimental procedure can be deposited as supplementary material, if it is not possible to publish them along with the text.