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Kaempferol protects HIT-T15 pancreatic beta cells from 2-deoxy-D-ribose-induced oxidative damage
During the progression of Type 2 diabetes, glucose toxicity is likely to contribute importantly to progressive beta cell failure. Oxidative stress is an important aspect of glucose toxicity in pancreatic beta cells, and reducing sugars, such as 2‐deoxy‐D‐ribose (dRib), produce reactive oxygen specie...
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Published in: | Phytotherapy research 2010-03, Vol.24 (3), p.419-423 |
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container_title | Phytotherapy research |
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description | During the progression of Type 2 diabetes, glucose toxicity is likely to contribute importantly to progressive beta cell failure. Oxidative stress is an important aspect of glucose toxicity in pancreatic beta cells, and reducing sugars, such as 2‐deoxy‐D‐ribose (dRib), produce reactive oxygen species. Furthermore, many of the biological properties of flavonoids are likely to be related to their antioxidant and free‐radical scavenging abilities. Accordingly, in the present study, we investigated whether kaempferol (a flavonol) protects beta cells from dRib‐induced oxidative damage. HIT‐T15 cells were cultured with various concentrations of dRib for 24h. Cell survivals, amounts of reactive oxygen species (ROS) generated, apoptosis, and lipid peroxidation were measured. dRib was found to dose‐dependently reduce cell survival and to markedly increase intracellular ROS levels, apoptosis, and lipid peroxidation. However, kaempferol (10 µM) suppressed dRib (20 mM) induced intracellular ROS, apoptosis, and lipid peroxidation. So, we demonstrate that kaempferol reduces dRib‐mediated beta cell damage interfering with ROS metabolism and protective effects against lipid peroxidation. Our findings indicate that kaempferol protects HIT‐T15 cells from dRib‐induced associated oxidative damage. Copyright © 2009 John Wiley & Sons, Ltd. |
doi_str_mv | 10.1002/ptr.2983 |
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Oxidative stress is an important aspect of glucose toxicity in pancreatic beta cells, and reducing sugars, such as 2‐deoxy‐D‐ribose (dRib), produce reactive oxygen species. Furthermore, many of the biological properties of flavonoids are likely to be related to their antioxidant and free‐radical scavenging abilities. Accordingly, in the present study, we investigated whether kaempferol (a flavonol) protects beta cells from dRib‐induced oxidative damage. HIT‐T15 cells were cultured with various concentrations of dRib for 24h. Cell survivals, amounts of reactive oxygen species (ROS) generated, apoptosis, and lipid peroxidation were measured. dRib was found to dose‐dependently reduce cell survival and to markedly increase intracellular ROS levels, apoptosis, and lipid peroxidation. However, kaempferol (10 µM) suppressed dRib (20 mM) induced intracellular ROS, apoptosis, and lipid peroxidation. So, we demonstrate that kaempferol reduces dRib‐mediated beta cell damage interfering with ROS metabolism and protective effects against lipid peroxidation. Our findings indicate that kaempferol protects HIT‐T15 cells from dRib‐induced associated oxidative damage. Copyright © 2009 John Wiley & Sons, Ltd.</description><identifier>ISSN: 0951-418X</identifier><identifier>EISSN: 1099-1573</identifier><identifier>DOI: 10.1002/ptr.2983</identifier><identifier>PMID: 19827031</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>2-deoxy-D-ribose ; Antioxidants - pharmacology ; Apoptosis ; Biological and medical sciences ; Cell Line ; Cell Survival ; Deoxyribose ; diabetes mellitus ; diabetes mellitus, Type 2 ; General pharmacology ; Humans ; Insulin-Secreting Cells - drug effects ; Kaempferols - pharmacology ; Lipid Peroxidation ; Medical sciences ; oxidative stress ; Oxidative Stress - drug effects ; Pharmacognosy. Homeopathy. Health food ; Pharmacology. Drug treatments ; Reactive Oxygen Species - metabolism ; Type 2</subject><ispartof>Phytotherapy research, 2010-03, Vol.24 (3), p.419-423</ispartof><rights>Copyright © 2009 John Wiley & Sons, Ltd.</rights><rights>2015 INIST-CNRS</rights><rights>(c) 2009 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4883-e8bf524df788230423a1834c991aaad53876b0f0d2dccffe5450908c463b0adb3</citedby><cites>FETCH-LOGICAL-c4883-e8bf524df788230423a1834c991aaad53876b0f0d2dccffe5450908c463b0adb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22409805$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19827031$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Yun Jung</creatorcontrib><creatorcontrib>Suh, Kwang Sik</creatorcontrib><creatorcontrib>Choi, Moon Chan</creatorcontrib><creatorcontrib>Chon, Suk</creatorcontrib><creatorcontrib>Oh, Seungjoon</creatorcontrib><creatorcontrib>Woo, Jeong-Taek</creatorcontrib><creatorcontrib>Kim, Sung-Woon</creatorcontrib><creatorcontrib>Kim, Jin-Woo</creatorcontrib><creatorcontrib>Kim, Young Seol</creatorcontrib><title>Kaempferol protects HIT-T15 pancreatic beta cells from 2-deoxy-D-ribose-induced oxidative damage</title><title>Phytotherapy research</title><addtitle>Phytother. Res</addtitle><description>During the progression of Type 2 diabetes, glucose toxicity is likely to contribute importantly to progressive beta cell failure. Oxidative stress is an important aspect of glucose toxicity in pancreatic beta cells, and reducing sugars, such as 2‐deoxy‐D‐ribose (dRib), produce reactive oxygen species. Furthermore, many of the biological properties of flavonoids are likely to be related to their antioxidant and free‐radical scavenging abilities. Accordingly, in the present study, we investigated whether kaempferol (a flavonol) protects beta cells from dRib‐induced oxidative damage. HIT‐T15 cells were cultured with various concentrations of dRib for 24h. Cell survivals, amounts of reactive oxygen species (ROS) generated, apoptosis, and lipid peroxidation were measured. dRib was found to dose‐dependently reduce cell survival and to markedly increase intracellular ROS levels, apoptosis, and lipid peroxidation. However, kaempferol (10 µM) suppressed dRib (20 mM) induced intracellular ROS, apoptosis, and lipid peroxidation. So, we demonstrate that kaempferol reduces dRib‐mediated beta cell damage interfering with ROS metabolism and protective effects against lipid peroxidation. Our findings indicate that kaempferol protects HIT‐T15 cells from dRib‐induced associated oxidative damage. Copyright © 2009 John Wiley & Sons, Ltd.</description><subject>2-deoxy-D-ribose</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Cell Survival</subject><subject>Deoxyribose</subject><subject>diabetes mellitus</subject><subject>diabetes mellitus, Type 2</subject><subject>General pharmacology</subject><subject>Humans</subject><subject>Insulin-Secreting Cells - drug effects</subject><subject>Kaempferols - pharmacology</subject><subject>Lipid Peroxidation</subject><subject>Medical sciences</subject><subject>oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Pharmacognosy. Homeopathy. Health food</subject><subject>Pharmacology. Drug treatments</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Type 2</subject><issn>0951-418X</issn><issn>1099-1573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNp10E1v1DAQgGELgei2IPUXVL4gcXEZf23sIxT6RYFSLQL14jr2GAWSJrJT2P33TbVROXGayzMz0kvIPodDDiDeDGM-FNbIJ2TBwVrGdSWfkgVYzZni5scO2S3lFwBYAeo52eHWiAokX5Cbjx67IWHuWzrkfsQwFnp6tmIrrungb0NGPzaB1jh6GrBtC02576hgEfv1hr1nuan7gqy5jXcBI-3XTZw2_iCNvvM_8QV5lnxb8OU898i34w-ro1N28eXk7OjtBQvKGMnQ1EkLFVNljJCghPTcSBWs5d77qKWpljUkiCKGkBJqpcGCCWopa_Cxlnvk9fZuyH0pGZMbctP5vHEc3EMkN0VyD5EmerClw13dYfwH5yoTeDUDX4JvU546NOXRCaHAGtCTY1v3t2lx89-H7nJ1NT-efVNGXD96n3-7ZSUr7b5_PnHX78Snr5fq3F3JezInjMk</recordid><startdate>201003</startdate><enddate>201003</enddate><creator>Lee, Yun Jung</creator><creator>Suh, Kwang Sik</creator><creator>Choi, Moon Chan</creator><creator>Chon, Suk</creator><creator>Oh, Seungjoon</creator><creator>Woo, Jeong-Taek</creator><creator>Kim, Sung-Woon</creator><creator>Kim, Jin-Woo</creator><creator>Kim, Young Seol</creator><general>John Wiley & Sons, Ltd</general><general>Wiley</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>201003</creationdate><title>Kaempferol protects HIT-T15 pancreatic beta cells from 2-deoxy-D-ribose-induced oxidative damage</title><author>Lee, Yun Jung ; Suh, Kwang Sik ; Choi, Moon Chan ; Chon, Suk ; Oh, Seungjoon ; Woo, Jeong-Taek ; Kim, Sung-Woon ; Kim, Jin-Woo ; Kim, Young Seol</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4883-e8bf524df788230423a1834c991aaad53876b0f0d2dccffe5450908c463b0adb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>2-deoxy-D-ribose</topic><topic>Antioxidants - pharmacology</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Cell Line</topic><topic>Cell Survival</topic><topic>Deoxyribose</topic><topic>diabetes mellitus</topic><topic>diabetes mellitus, Type 2</topic><topic>General pharmacology</topic><topic>Humans</topic><topic>Insulin-Secreting Cells - drug effects</topic><topic>Kaempferols - pharmacology</topic><topic>Lipid Peroxidation</topic><topic>Medical sciences</topic><topic>oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Pharmacognosy. Homeopathy. Health food</topic><topic>Pharmacology. Drug treatments</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Type 2</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Yun Jung</creatorcontrib><creatorcontrib>Suh, Kwang Sik</creatorcontrib><creatorcontrib>Choi, Moon Chan</creatorcontrib><creatorcontrib>Chon, Suk</creatorcontrib><creatorcontrib>Oh, Seungjoon</creatorcontrib><creatorcontrib>Woo, Jeong-Taek</creatorcontrib><creatorcontrib>Kim, Sung-Woon</creatorcontrib><creatorcontrib>Kim, Jin-Woo</creatorcontrib><creatorcontrib>Kim, Young Seol</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Phytotherapy research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Yun Jung</au><au>Suh, Kwang Sik</au><au>Choi, Moon Chan</au><au>Chon, Suk</au><au>Oh, Seungjoon</au><au>Woo, Jeong-Taek</au><au>Kim, Sung-Woon</au><au>Kim, Jin-Woo</au><au>Kim, Young Seol</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Kaempferol protects HIT-T15 pancreatic beta cells from 2-deoxy-D-ribose-induced oxidative damage</atitle><jtitle>Phytotherapy research</jtitle><addtitle>Phytother. Res</addtitle><date>2010-03</date><risdate>2010</risdate><volume>24</volume><issue>3</issue><spage>419</spage><epage>423</epage><pages>419-423</pages><issn>0951-418X</issn><eissn>1099-1573</eissn><abstract>During the progression of Type 2 diabetes, glucose toxicity is likely to contribute importantly to progressive beta cell failure. Oxidative stress is an important aspect of glucose toxicity in pancreatic beta cells, and reducing sugars, such as 2‐deoxy‐D‐ribose (dRib), produce reactive oxygen species. Furthermore, many of the biological properties of flavonoids are likely to be related to their antioxidant and free‐radical scavenging abilities. Accordingly, in the present study, we investigated whether kaempferol (a flavonol) protects beta cells from dRib‐induced oxidative damage. HIT‐T15 cells were cultured with various concentrations of dRib for 24h. Cell survivals, amounts of reactive oxygen species (ROS) generated, apoptosis, and lipid peroxidation were measured. dRib was found to dose‐dependently reduce cell survival and to markedly increase intracellular ROS levels, apoptosis, and lipid peroxidation. However, kaempferol (10 µM) suppressed dRib (20 mM) induced intracellular ROS, apoptosis, and lipid peroxidation. So, we demonstrate that kaempferol reduces dRib‐mediated beta cell damage interfering with ROS metabolism and protective effects against lipid peroxidation. Our findings indicate that kaempferol protects HIT‐T15 cells from dRib‐induced associated oxidative damage. Copyright © 2009 John Wiley & Sons, Ltd.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>19827031</pmid><doi>10.1002/ptr.2983</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 2-deoxy-D-ribose Antioxidants - pharmacology Apoptosis Biological and medical sciences Cell Line Cell Survival Deoxyribose diabetes mellitus diabetes mellitus, Type 2 General pharmacology Humans Insulin-Secreting Cells - drug effects Kaempferols - pharmacology Lipid Peroxidation Medical sciences oxidative stress Oxidative Stress - drug effects Pharmacognosy. Homeopathy. Health food Pharmacology. Drug treatments Reactive Oxygen Species - metabolism Type 2 |
title | Kaempferol protects HIT-T15 pancreatic beta cells from 2-deoxy-D-ribose-induced oxidative damage |
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