Hyperoside mediates protection from diabetes kidney disease by regulating ROS‐ERK signaling pathway and pyroptosis
Renal tubular injury is a key factor in the progression of diabetic kidney disease to end‐stage renal disease. Hyperoside, a natural flavonol glycoside in various plants, is a potentially effective drug for the clinical treatment of diabetic kidney disease. However, the specific mechanisms remain un...
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| Veröffentlicht in: | Phytotherapy research 2023-12, Vol.37 (12), p.5871-5882 |
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| creator | Zhang, Kejia Li, MiaoMiao Yin, Kaiwen Wang, Minjie Dong, Qiuchi Miao, Zilan Guan, Yubo Wu, Qi Zhou, Yao |
| description | Renal tubular injury is a key factor in the progression of diabetic kidney disease to end‐stage renal disease. Hyperoside, a natural flavonol glycoside in various plants, is a potentially effective drug for the clinical treatment of diabetic kidney disease. However, the specific mechanisms remain unknown. Therefore, this study will explore the effect and mechanism of hyperoside on renal tubulointerstitium in diabetic kidney disease. db/db mouse (C57BL/KsJ) is a model of type 2 diabetes resulting from Leptin receptor point mutations, with the appearance of diabetic kidney disease. Therefore, db/db mice were used for in vivo experimental studies. In vitro, human renal tubular epithelial cells were incubated with bovine serum albumin to simulate the injury of renal tubular epithelial cells caused by excessive albumin in primary urine. The experimental results showed that hyperoside could improve kidney function and reduce kidney tissue damage in mice, and could inhibit oxidative stress, extracellularly regulated protein kinases 1/2 signaling activation, and pyroptosis in human renal tubular epithelial cells. Therefore, hyperoside inhibited oxidative stress by regulating the activation of the extracellularly regulated protein kinases 1/2/mitogen‐activated protein kinase signaling pathway, thereby alleviating proteinuria‐induced pyroptosis in renal tubular epithelial cells. This study provides novel evidence that could facilitate the clinical application of hyperoside in diabetic kidney disease treatment.
Experimental design and mechanism diagram |
| doi_str_mv | 10.1002/ptr.7993 |
| format | Article |
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Experimental design and mechanism diagram</description><identifier>ISSN: 0951-418X</identifier><identifier>EISSN: 1099-1573</identifier><identifier>DOI: 10.1002/ptr.7993</identifier><identifier>PMID: 37646382</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Animal tissues ; Animals ; Bovine serum albumin ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetes Mellitus, Type 2 - metabolism ; diabetic kidney disease ; Diabetic Nephropathies - drug therapy ; Epithelial cells ; Epithelium ; Flavonols ; Health services ; Humans ; hyperoside ; In vivo methods and tests ; Kidney ; Kidney diseases ; Kidneys ; Kinases ; Medical treatment ; Mice ; Mice, Inbred C57BL ; Oxidative stress ; Protein kinase ; Protein Kinases - metabolism ; Proteins ; Proteinuria ; Pyroptosis ; Reactive Oxygen Species - metabolism ; renal tubular epithelial cell pyroptosis ; Serum albumin ; Signal Transduction</subject><ispartof>Phytotherapy research, 2023-12, Vol.37 (12), p.5871-5882</ispartof><rights>2023 John Wiley & Sons Ltd.</rights><rights>2023 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3103-88a028b98cadd15366ee6189ba14c15ca69b7cdec2b42b9441e0529e72431d413</cites><orcidid>0009-0001-7225-3125 ; 0009-0007-5263-6587 ; 0009-0005-5035-0935 ; 0009-0000-8763-8477 ; 0000-0002-6970-8571 ; 0009-0009-8499-6004 ; 0000-0002-0537-6467 ; 0000-0002-2845-6339</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fptr.7993$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fptr.7993$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37646382$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Kejia</creatorcontrib><creatorcontrib>Li, MiaoMiao</creatorcontrib><creatorcontrib>Yin, Kaiwen</creatorcontrib><creatorcontrib>Wang, Minjie</creatorcontrib><creatorcontrib>Dong, Qiuchi</creatorcontrib><creatorcontrib>Miao, Zilan</creatorcontrib><creatorcontrib>Guan, Yubo</creatorcontrib><creatorcontrib>Wu, Qi</creatorcontrib><creatorcontrib>Zhou, Yao</creatorcontrib><title>Hyperoside mediates protection from diabetes kidney disease by regulating ROS‐ERK signaling pathway and pyroptosis</title><title>Phytotherapy research</title><addtitle>Phytother Res</addtitle><description>Renal tubular injury is a key factor in the progression of diabetic kidney disease to end‐stage renal disease. Hyperoside, a natural flavonol glycoside in various plants, is a potentially effective drug for the clinical treatment of diabetic kidney disease. However, the specific mechanisms remain unknown. Therefore, this study will explore the effect and mechanism of hyperoside on renal tubulointerstitium in diabetic kidney disease. db/db mouse (C57BL/KsJ) is a model of type 2 diabetes resulting from Leptin receptor point mutations, with the appearance of diabetic kidney disease. Therefore, db/db mice were used for in vivo experimental studies. In vitro, human renal tubular epithelial cells were incubated with bovine serum albumin to simulate the injury of renal tubular epithelial cells caused by excessive albumin in primary urine. The experimental results showed that hyperoside could improve kidney function and reduce kidney tissue damage in mice, and could inhibit oxidative stress, extracellularly regulated protein kinases 1/2 signaling activation, and pyroptosis in human renal tubular epithelial cells. Therefore, hyperoside inhibited oxidative stress by regulating the activation of the extracellularly regulated protein kinases 1/2/mitogen‐activated protein kinase signaling pathway, thereby alleviating proteinuria‐induced pyroptosis in renal tubular epithelial cells. This study provides novel evidence that could facilitate the clinical application of hyperoside in diabetic kidney disease treatment.
Experimental design and mechanism diagram</description><subject>Animal tissues</subject><subject>Animals</subject><subject>Bovine serum albumin</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>diabetic kidney disease</subject><subject>Diabetic Nephropathies - drug therapy</subject><subject>Epithelial cells</subject><subject>Epithelium</subject><subject>Flavonols</subject><subject>Health services</subject><subject>Humans</subject><subject>hyperoside</subject><subject>In vivo methods and tests</subject><subject>Kidney</subject><subject>Kidney diseases</subject><subject>Kidneys</subject><subject>Kinases</subject><subject>Medical treatment</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Oxidative stress</subject><subject>Protein kinase</subject><subject>Protein Kinases - metabolism</subject><subject>Proteins</subject><subject>Proteinuria</subject><subject>Pyroptosis</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>renal tubular epithelial cell pyroptosis</subject><subject>Serum albumin</subject><subject>Signal Transduction</subject><issn>0951-418X</issn><issn>1099-1573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kctKxDAUhoMoOl7AJ5CAGzfV3NomS5HxgoIyKrgraXpmjHbamqRIdz6Cz-iTmPEKgquQk48_nO9HaJuSfUoIO-iC28-V4ktoRIlSCU1zvoxGRKU0EVTeraF17x8IIYoRsYrWeJ6JjEs2QuF06MC13laA51BZHcDjzrUBTLBtg6euneM4LmHx8GirBoZ496A94HLADmZ9rYNtZnhyef328jqenGNvZ42uF7NOh_tnPWDdVLgbXNuF-JXfRCtTXXvY-jo30O3x-OboNLm4PDk7OrxIDKeEJ1JqwmSppNFVRVOeZQAZlarUVBiaGp2pMjcVGFYKViohKJCUKciZ4LQSlG-gvc_cuNBTDz4Uc-sN1LVuoO19wWQqozUhRUR3_6APbe_iFpFS0VuWMUJ-A01U5h1Mi87ZuXZDQUmxaKKITRSLJiK68xXYl1HsD_itPgLJJ_Bsaxj-DSqubiYfge9i8JQ_</recordid><startdate>202312</startdate><enddate>202312</enddate><creator>Zhang, Kejia</creator><creator>Li, MiaoMiao</creator><creator>Yin, Kaiwen</creator><creator>Wang, Minjie</creator><creator>Dong, Qiuchi</creator><creator>Miao, Zilan</creator><creator>Guan, Yubo</creator><creator>Wu, Qi</creator><creator>Zhou, Yao</creator><general>John Wiley & Sons, Ltd</general><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0009-0001-7225-3125</orcidid><orcidid>https://orcid.org/0009-0007-5263-6587</orcidid><orcidid>https://orcid.org/0009-0005-5035-0935</orcidid><orcidid>https://orcid.org/0009-0000-8763-8477</orcidid><orcidid>https://orcid.org/0000-0002-6970-8571</orcidid><orcidid>https://orcid.org/0009-0009-8499-6004</orcidid><orcidid>https://orcid.org/0000-0002-0537-6467</orcidid><orcidid>https://orcid.org/0000-0002-2845-6339</orcidid></search><sort><creationdate>202312</creationdate><title>Hyperoside mediates protection from diabetes kidney disease by regulating ROS‐ERK signaling pathway and pyroptosis</title><author>Zhang, Kejia ; Li, MiaoMiao ; Yin, Kaiwen ; Wang, Minjie ; Dong, Qiuchi ; Miao, Zilan ; Guan, Yubo ; Wu, Qi ; Zhou, Yao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3103-88a028b98cadd15366ee6189ba14c15ca69b7cdec2b42b9441e0529e72431d413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animal tissues</topic><topic>Animals</topic><topic>Bovine serum albumin</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>diabetic kidney disease</topic><topic>Diabetic Nephropathies - drug therapy</topic><topic>Epithelial cells</topic><topic>Epithelium</topic><topic>Flavonols</topic><topic>Health services</topic><topic>Humans</topic><topic>hyperoside</topic><topic>In vivo methods and tests</topic><topic>Kidney</topic><topic>Kidney diseases</topic><topic>Kidneys</topic><topic>Kinases</topic><topic>Medical treatment</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Oxidative stress</topic><topic>Protein kinase</topic><topic>Protein Kinases - metabolism</topic><topic>Proteins</topic><topic>Proteinuria</topic><topic>Pyroptosis</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>renal tubular epithelial cell pyroptosis</topic><topic>Serum albumin</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Kejia</creatorcontrib><creatorcontrib>Li, MiaoMiao</creatorcontrib><creatorcontrib>Yin, Kaiwen</creatorcontrib><creatorcontrib>Wang, Minjie</creatorcontrib><creatorcontrib>Dong, Qiuchi</creatorcontrib><creatorcontrib>Miao, Zilan</creatorcontrib><creatorcontrib>Guan, Yubo</creatorcontrib><creatorcontrib>Wu, Qi</creatorcontrib><creatorcontrib>Zhou, Yao</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Phytotherapy research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Kejia</au><au>Li, MiaoMiao</au><au>Yin, Kaiwen</au><au>Wang, Minjie</au><au>Dong, Qiuchi</au><au>Miao, Zilan</au><au>Guan, Yubo</au><au>Wu, Qi</au><au>Zhou, Yao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperoside mediates protection from diabetes kidney disease by regulating ROS‐ERK signaling pathway and pyroptosis</atitle><jtitle>Phytotherapy research</jtitle><addtitle>Phytother Res</addtitle><date>2023-12</date><risdate>2023</risdate><volume>37</volume><issue>12</issue><spage>5871</spage><epage>5882</epage><pages>5871-5882</pages><issn>0951-418X</issn><eissn>1099-1573</eissn><abstract>Renal tubular injury is a key factor in the progression of diabetic kidney disease to end‐stage renal disease. Hyperoside, a natural flavonol glycoside in various plants, is a potentially effective drug for the clinical treatment of diabetic kidney disease. However, the specific mechanisms remain unknown. Therefore, this study will explore the effect and mechanism of hyperoside on renal tubulointerstitium in diabetic kidney disease. db/db mouse (C57BL/KsJ) is a model of type 2 diabetes resulting from Leptin receptor point mutations, with the appearance of diabetic kidney disease. Therefore, db/db mice were used for in vivo experimental studies. In vitro, human renal tubular epithelial cells were incubated with bovine serum albumin to simulate the injury of renal tubular epithelial cells caused by excessive albumin in primary urine. The experimental results showed that hyperoside could improve kidney function and reduce kidney tissue damage in mice, and could inhibit oxidative stress, extracellularly regulated protein kinases 1/2 signaling activation, and pyroptosis in human renal tubular epithelial cells. Therefore, hyperoside inhibited oxidative stress by regulating the activation of the extracellularly regulated protein kinases 1/2/mitogen‐activated protein kinase signaling pathway, thereby alleviating proteinuria‐induced pyroptosis in renal tubular epithelial cells. This study provides novel evidence that could facilitate the clinical application of hyperoside in diabetic kidney disease treatment.
Experimental design and mechanism diagram</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>37646382</pmid><doi>10.1002/ptr.7993</doi><tpages>12</tpages><orcidid>https://orcid.org/0009-0001-7225-3125</orcidid><orcidid>https://orcid.org/0009-0007-5263-6587</orcidid><orcidid>https://orcid.org/0009-0005-5035-0935</orcidid><orcidid>https://orcid.org/0009-0000-8763-8477</orcidid><orcidid>https://orcid.org/0000-0002-6970-8571</orcidid><orcidid>https://orcid.org/0009-0009-8499-6004</orcidid><orcidid>https://orcid.org/0000-0002-0537-6467</orcidid><orcidid>https://orcid.org/0000-0002-2845-6339</orcidid></addata></record> |
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| subjects | Animal tissues Animals Bovine serum albumin Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - metabolism diabetic kidney disease Diabetic Nephropathies - drug therapy Epithelial cells Epithelium Flavonols Health services Humans hyperoside In vivo methods and tests Kidney Kidney diseases Kidneys Kinases Medical treatment Mice Mice, Inbred C57BL Oxidative stress Protein kinase Protein Kinases - metabolism Proteins Proteinuria Pyroptosis Reactive Oxygen Species - metabolism renal tubular epithelial cell pyroptosis Serum albumin Signal Transduction |
| title | Hyperoside mediates protection from diabetes kidney disease by regulating ROS‐ERK signaling pathway and pyroptosis |
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