Quercetin improves diabetic kidney disease by inhibiting ferroptosis and regulating the Nrf2 in streptozotocin-induced diabetic rats

Diabetic kidney disease (DKD) is a leading factor in end-stage renal disease. The complexity of its pathogenesis, combined with the limited treatment efficacy, necessitates deeper insights into potential causes. Studies suggest that ferroptosis-driven renal tubular damage contributes to DKD's p...

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Vydáno v:Renal failure Ročník 46; číslo 1; s. 2327495
Hlavní autoři: Zhang, Lei, Wang, Xingzhi, Chang, Liang, Ren, Yiqun, Sui, Manshu, Fu, Yuting, Hao, Lirong
Médium: Journal Article
Jazyk:angličtina
Vydáno: England Taylor & Francis Ltd 01.12.2024
Taylor & Francis
Taylor & Francis Group
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ISSN:0886-022X, 1525-6049, 1525-6049
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Shrnutí:Diabetic kidney disease (DKD) is a leading factor in end-stage renal disease. The complexity of its pathogenesis, combined with the limited treatment efficacy, necessitates deeper insights into potential causes. Studies suggest that ferroptosis-driven renal tubular damage contributes to DKD's progression, making its counteraction a potential therapeutic strategy. Quercetin, a flavonoid found in numerous fruits and vegetables, has demonstrated DKD mitigation in mouse models, though its protective mechanism remains ambiguous. In this study, we delved into quercetin's potential anti-ferroptotic properties, employing a DKD rat model and high glucose (HG)-treated renal tubular epithelial cell models. Our findings revealed that HG prompted unusual ferroptosis activation in renal tubular epithelial cells. However, quercetin counteracted this by inhibiting ferroptosis and activating NFE2-related factor 2 (Nrf2) expression in both DKD rats and HG-treated HK-2 cells, indicating its renal protective role. Further experiments, both and , validated that quercetin stimulates Nrf2. Thus, our research underscores quercetin's potential in DKD treatment by modulating the ferroptosis process activating Nrf2 in a distinct DKD rat model, offering a fresh perspective on quercetin's protective mechanisms.
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These author contributed to this work as a senior author.
ISSN:0886-022X
1525-6049
1525-6049
DOI:10.1080/0886022X.2024.2327495