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 |
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| Médium: | Journal Article |
| Jazyk: | angličtina |
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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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| Abstract | 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. |
|---|---|
| AbstractList | 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 in vivo and in vitro, validated that quercetin stimulates Nrf2. Thus, our research underscores quercetin's potential in DKD treatment by modulating the ferroptosis process via activating Nrf2 in a distinct DKD rat model, offering a fresh perspective on quercetin's protective mechanisms.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 in vivo and in vitro, validated that quercetin stimulates Nrf2. Thus, our research underscores quercetin's potential in DKD treatment by modulating the ferroptosis process via activating Nrf2 in a distinct DKD rat model, offering a fresh perspective on quercetin's protective mechanisms. 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 in vivo and in vitro, validated that quercetin stimulates Nrf2. Thus, our research underscores quercetin’s potential in DKD treatment by modulating the ferroptosis process via activating Nrf2 in a distinct DKD rat model, offering a fresh perspective on quercetin’s protective mechanisms. 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. |
| Author | Fu, Yuting Sui, Manshu Ren, Yiqun Hao, Lirong Wang, Xingzhi Chang, Liang Zhang, Lei |
| Author_xml | – sequence: 1 givenname: Lei surname: Zhang fullname: Zhang, Lei organization: Department of Nephropathy and Hemodialysis, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China – sequence: 2 givenname: Xingzhi surname: Wang fullname: Wang, Xingzhi organization: Department of Nephropathy and Hemodialysis, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China – sequence: 3 givenname: Liang surname: Chang fullname: Chang, Liang organization: Department of Nephropathy and Hemodialysis, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China – sequence: 4 givenname: Yiqun surname: Ren fullname: Ren, Yiqun organization: Department of Pathology, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China – sequence: 5 givenname: Manshu surname: Sui fullname: Sui, Manshu organization: Department of Nephropathy and Hemodialysis, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China – sequence: 6 givenname: Yuting surname: Fu fullname: Fu, Yuting organization: Department of Nephropathy and Hemodialysis, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China – sequence: 7 givenname: Lirong surname: Hao fullname: Hao, Lirong organization: Department of Nephropathy and Hemodialysis, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China, Department of Nephropathy, Southern University of Science and Technology Hospital, Shenzhen, China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38465879$$D View this record in MEDLINE/PubMed |
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| Keywords | Diabetic kidney disease (DKD) quercetin ferroptosis rat streptozotocin Nrf2 |
| Language | English |
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| Snippet | Diabetic kidney disease (DKD) is a leading factor in end-stage renal disease. The complexity of its pathogenesis, combined with the limited treatment efficacy,... |
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| StartPage | 2327495 |
| SubjectTerms | Animal models Basic Sciences Investigations Cell activation Cell culture Diabetes Diabetes mellitus Diabetic kidney disease (DKD) End-stage renal disease Epithelial cells Ferroptosis Flavonoids Kidney diseases Nrf2 Quercetin rat Streptozocin streptozotocin |
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| Title | Quercetin improves diabetic kidney disease by inhibiting ferroptosis and regulating the Nrf2 in streptozotocin-induced diabetic rats |
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