Celastrol pretreatment as a therapeutic option against cisplatin-induced nephrotoxicity
Celastrol is a natural bioactive compound extracted from the medicinal plant Tripterygium wilfordii Hook F. It exhibits immunosuppressive, anti-inflammatory, and antioxidant activities. Cisplatin is a commonly used chemotherapeutic drug in the treatment of a wide range of tumors. Although very effec...
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| Veröffentlicht in: | Toxicology research (Cambridge) 2019-09, Vol.8 (5), p.723-73 |
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| creator | Boran, Tugce Gunaydin, Aysenur Jannuzzi, Ayse Tarbin Ozcagli, Eren Alpertunga, Buket |
| description | Celastrol is a natural bioactive compound extracted from the medicinal plant
Tripterygium wilfordii
Hook F. It exhibits immunosuppressive, anti-inflammatory, and antioxidant activities. Cisplatin is a commonly used chemotherapeutic drug in the treatment of a wide range of tumors. Although very effective therapeutically, it can cause nephrotoxicity leading to dose reduction or discontinuation of treatment. This study aims to clarify the therapeutic potential of celastrol in cisplatin-induced nephrotoxicity. The possible protective effects of celastrol pretreatment against cisplatin-induced oxidative stress and genotoxicity were investigated. A rat kidney epithelial cell line NRK-52E was pretreated with the desired concentrations of celastrol (200 nM, 100 nM, and 50 nM) for 24 h. The cells were treated with 50 μM cisplatin for a further 24 h to see whether cisplatin caused the same or less toxicity compared to the vehicle control group. Alkaline comet assay was performed for genotoxicity assessment. Genotoxicity evaluation revealed that celastrol caused a statistically significant reduction in DNA damage. Oxidative stress parameters were evaluated by measuring the glutathione (GSH) and protein carbonyl (PC) levels and also by measuring the enzyme activities of glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT) and superoxide dismutase (SOD) enzymes. Celastrol pretreatment increased the GSH content of the cells and ameliorated the protein carbonylation level. Likewise, celastrol pretreatment improved the GR and CAT activities. However, no significant difference was observed in GPx and SOD activities. In the light of these findings, celastrol treatment could be a therapeutic option to reduce cisplatin-induced nephrotoxicity. Further studies are needed for the clarification of its therapeutic potential.
Celastrol is a natural bioactive compound extracted from the medicinal plant
Tripterygium wilfordii
Hook F. |
| doi_str_mv | 10.1039/c9tx00141g |
| format | Article |
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Tripterygium wilfordii
Hook F. It exhibits immunosuppressive, anti-inflammatory, and antioxidant activities. Cisplatin is a commonly used chemotherapeutic drug in the treatment of a wide range of tumors. Although very effective therapeutically, it can cause nephrotoxicity leading to dose reduction or discontinuation of treatment. This study aims to clarify the therapeutic potential of celastrol in cisplatin-induced nephrotoxicity. The possible protective effects of celastrol pretreatment against cisplatin-induced oxidative stress and genotoxicity were investigated. A rat kidney epithelial cell line NRK-52E was pretreated with the desired concentrations of celastrol (200 nM, 100 nM, and 50 nM) for 24 h. The cells were treated with 50 μM cisplatin for a further 24 h to see whether cisplatin caused the same or less toxicity compared to the vehicle control group. Alkaline comet assay was performed for genotoxicity assessment. Genotoxicity evaluation revealed that celastrol caused a statistically significant reduction in DNA damage. Oxidative stress parameters were evaluated by measuring the glutathione (GSH) and protein carbonyl (PC) levels and also by measuring the enzyme activities of glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT) and superoxide dismutase (SOD) enzymes. Celastrol pretreatment increased the GSH content of the cells and ameliorated the protein carbonylation level. Likewise, celastrol pretreatment improved the GR and CAT activities. However, no significant difference was observed in GPx and SOD activities. In the light of these findings, celastrol treatment could be a therapeutic option to reduce cisplatin-induced nephrotoxicity. Further studies are needed for the clarification of its therapeutic potential.
Celastrol is a natural bioactive compound extracted from the medicinal plant
Tripterygium wilfordii
Hook F.</description><identifier>ISSN: 2045-452X</identifier><identifier>ISSN: 2045-4538</identifier><identifier>EISSN: 2045-4538</identifier><identifier>DOI: 10.1039/c9tx00141g</identifier><identifier>PMID: 31588349</identifier><language>eng</language><publisher>England: Royal Society of Chemistry</publisher><subject>Antioxidants ; Bioactive compounds ; Bioassays ; Biocompatibility ; Carbonyl compounds ; Carbonyls ; Catalase ; Chemistry ; Cisplatin ; Comet assay ; Damage assessment ; Damage detection ; DNA damage ; Enzymatic activity ; Epithelial cells ; Genotoxicity ; Glutathione ; Glutathione peroxidase ; Glutathione reductase ; Herbal medicine ; Inflammation ; Kidneys ; Medicinal plants ; Oxidative stress ; Peroxidase ; Plant extracts ; Pretreatment ; Proteins ; Reductases ; Reduction ; Statistical analysis ; Superoxide dismutase ; Toxicity ; Tumors</subject><ispartof>Toxicology research (Cambridge), 2019-09, Vol.8 (5), p.723-73</ispartof><rights>This journal is © The Royal Society of Chemistry 2019.</rights><rights>Copyright Royal Society of Chemistry 2019</rights><rights>This journal is © The Royal Society of Chemistry 2019 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c428t-81f00874837399eb96343a84f20b47d1c453b1454df1e70cbcb1b90ba1e26f3b3</citedby><cites>FETCH-LOGICAL-c428t-81f00874837399eb96343a84f20b47d1c453b1454df1e70cbcb1b90ba1e26f3b3</cites><orcidid>0000-0001-6043-7560</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6762010/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6762010/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31588349$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Boran, Tugce</creatorcontrib><creatorcontrib>Gunaydin, Aysenur</creatorcontrib><creatorcontrib>Jannuzzi, Ayse Tarbin</creatorcontrib><creatorcontrib>Ozcagli, Eren</creatorcontrib><creatorcontrib>Alpertunga, Buket</creatorcontrib><title>Celastrol pretreatment as a therapeutic option against cisplatin-induced nephrotoxicity</title><title>Toxicology research (Cambridge)</title><addtitle>Toxicol Res (Camb)</addtitle><description>Celastrol is a natural bioactive compound extracted from the medicinal plant
Tripterygium wilfordii
Hook F. It exhibits immunosuppressive, anti-inflammatory, and antioxidant activities. Cisplatin is a commonly used chemotherapeutic drug in the treatment of a wide range of tumors. Although very effective therapeutically, it can cause nephrotoxicity leading to dose reduction or discontinuation of treatment. This study aims to clarify the therapeutic potential of celastrol in cisplatin-induced nephrotoxicity. The possible protective effects of celastrol pretreatment against cisplatin-induced oxidative stress and genotoxicity were investigated. A rat kidney epithelial cell line NRK-52E was pretreated with the desired concentrations of celastrol (200 nM, 100 nM, and 50 nM) for 24 h. The cells were treated with 50 μM cisplatin for a further 24 h to see whether cisplatin caused the same or less toxicity compared to the vehicle control group. Alkaline comet assay was performed for genotoxicity assessment. Genotoxicity evaluation revealed that celastrol caused a statistically significant reduction in DNA damage. Oxidative stress parameters were evaluated by measuring the glutathione (GSH) and protein carbonyl (PC) levels and also by measuring the enzyme activities of glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT) and superoxide dismutase (SOD) enzymes. Celastrol pretreatment increased the GSH content of the cells and ameliorated the protein carbonylation level. Likewise, celastrol pretreatment improved the GR and CAT activities. However, no significant difference was observed in GPx and SOD activities. In the light of these findings, celastrol treatment could be a therapeutic option to reduce cisplatin-induced nephrotoxicity. Further studies are needed for the clarification of its therapeutic potential.
Celastrol is a natural bioactive compound extracted from the medicinal plant
Tripterygium wilfordii
Hook F.</description><subject>Antioxidants</subject><subject>Bioactive compounds</subject><subject>Bioassays</subject><subject>Biocompatibility</subject><subject>Carbonyl compounds</subject><subject>Carbonyls</subject><subject>Catalase</subject><subject>Chemistry</subject><subject>Cisplatin</subject><subject>Comet assay</subject><subject>Damage assessment</subject><subject>Damage detection</subject><subject>DNA damage</subject><subject>Enzymatic activity</subject><subject>Epithelial cells</subject><subject>Genotoxicity</subject><subject>Glutathione</subject><subject>Glutathione peroxidase</subject><subject>Glutathione reductase</subject><subject>Herbal medicine</subject><subject>Inflammation</subject><subject>Kidneys</subject><subject>Medicinal plants</subject><subject>Oxidative stress</subject><subject>Peroxidase</subject><subject>Plant extracts</subject><subject>Pretreatment</subject><subject>Proteins</subject><subject>Reductases</subject><subject>Reduction</subject><subject>Statistical analysis</subject><subject>Superoxide dismutase</subject><subject>Toxicity</subject><subject>Tumors</subject><issn>2045-452X</issn><issn>2045-4538</issn><issn>2045-4538</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNpdkc1r3DAQxUVpacI2l95TDL2EgtvRh235EghLvyDQS0N6E5I83lXwSq4kh-S_r8qmm6RzmYH58Xgzj5C3FD5S4P0n2-c7ACro5gU5ZiCaWjRcvjzM7NcROUnpBkp1wFrevCZHnDZSctEfk-s1TjrlGKZqjpgj6rxDnyudKl3lLUY945KdrcKcXfCV3mjnU66sS_Oks_O188Nicag8ztsYcrhz1uX7N-TVqKeEJw99Ra6-fP65_lZf_vj6fX1xWVvBZK4lHQFkJyTveN-j6VsuuJZiZGBEN1BbjjFUNGIYKXZgjTXU9GA0RdaO3PAVOd_rzovZ4WCL96gnNUe30_FeBe3U8413W7UJt6rtWgblgyty9iAQw-8FU1Y7lyxOk_YYlqQYByolsJ4W9P1_6E1Yoi_nKcYkCNHJVhbqw56yMaQUcTyYoaD-RqYeIyvwu6f2D-i_gApwugdisoftE4E_AdKdYw</recordid><startdate>20190901</startdate><enddate>20190901</enddate><creator>Boran, Tugce</creator><creator>Gunaydin, Aysenur</creator><creator>Jannuzzi, Ayse Tarbin</creator><creator>Ozcagli, Eren</creator><creator>Alpertunga, Buket</creator><general>Royal Society of Chemistry</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6043-7560</orcidid></search><sort><creationdate>20190901</creationdate><title>Celastrol pretreatment as a therapeutic option against cisplatin-induced nephrotoxicity</title><author>Boran, Tugce ; Gunaydin, Aysenur ; Jannuzzi, Ayse Tarbin ; Ozcagli, Eren ; Alpertunga, Buket</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c428t-81f00874837399eb96343a84f20b47d1c453b1454df1e70cbcb1b90ba1e26f3b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Antioxidants</topic><topic>Bioactive compounds</topic><topic>Bioassays</topic><topic>Biocompatibility</topic><topic>Carbonyl compounds</topic><topic>Carbonyls</topic><topic>Catalase</topic><topic>Chemistry</topic><topic>Cisplatin</topic><topic>Comet assay</topic><topic>Damage assessment</topic><topic>Damage detection</topic><topic>DNA damage</topic><topic>Enzymatic activity</topic><topic>Epithelial cells</topic><topic>Genotoxicity</topic><topic>Glutathione</topic><topic>Glutathione peroxidase</topic><topic>Glutathione reductase</topic><topic>Herbal medicine</topic><topic>Inflammation</topic><topic>Kidneys</topic><topic>Medicinal plants</topic><topic>Oxidative stress</topic><topic>Peroxidase</topic><topic>Plant extracts</topic><topic>Pretreatment</topic><topic>Proteins</topic><topic>Reductases</topic><topic>Reduction</topic><topic>Statistical analysis</topic><topic>Superoxide dismutase</topic><topic>Toxicity</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Boran, Tugce</creatorcontrib><creatorcontrib>Gunaydin, Aysenur</creatorcontrib><creatorcontrib>Jannuzzi, Ayse Tarbin</creatorcontrib><creatorcontrib>Ozcagli, Eren</creatorcontrib><creatorcontrib>Alpertunga, Buket</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Toxicology research (Cambridge)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Boran, Tugce</au><au>Gunaydin, Aysenur</au><au>Jannuzzi, Ayse Tarbin</au><au>Ozcagli, Eren</au><au>Alpertunga, Buket</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Celastrol pretreatment as a therapeutic option against cisplatin-induced nephrotoxicity</atitle><jtitle>Toxicology research (Cambridge)</jtitle><addtitle>Toxicol Res (Camb)</addtitle><date>2019-09-01</date><risdate>2019</risdate><volume>8</volume><issue>5</issue><spage>723</spage><epage>73</epage><pages>723-73</pages><issn>2045-452X</issn><issn>2045-4538</issn><eissn>2045-4538</eissn><abstract>Celastrol is a natural bioactive compound extracted from the medicinal plant
Tripterygium wilfordii
Hook F. It exhibits immunosuppressive, anti-inflammatory, and antioxidant activities. Cisplatin is a commonly used chemotherapeutic drug in the treatment of a wide range of tumors. Although very effective therapeutically, it can cause nephrotoxicity leading to dose reduction or discontinuation of treatment. This study aims to clarify the therapeutic potential of celastrol in cisplatin-induced nephrotoxicity. The possible protective effects of celastrol pretreatment against cisplatin-induced oxidative stress and genotoxicity were investigated. A rat kidney epithelial cell line NRK-52E was pretreated with the desired concentrations of celastrol (200 nM, 100 nM, and 50 nM) for 24 h. The cells were treated with 50 μM cisplatin for a further 24 h to see whether cisplatin caused the same or less toxicity compared to the vehicle control group. Alkaline comet assay was performed for genotoxicity assessment. Genotoxicity evaluation revealed that celastrol caused a statistically significant reduction in DNA damage. Oxidative stress parameters were evaluated by measuring the glutathione (GSH) and protein carbonyl (PC) levels and also by measuring the enzyme activities of glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT) and superoxide dismutase (SOD) enzymes. Celastrol pretreatment increased the GSH content of the cells and ameliorated the protein carbonylation level. Likewise, celastrol pretreatment improved the GR and CAT activities. However, no significant difference was observed in GPx and SOD activities. In the light of these findings, celastrol treatment could be a therapeutic option to reduce cisplatin-induced nephrotoxicity. Further studies are needed for the clarification of its therapeutic potential.
Celastrol is a natural bioactive compound extracted from the medicinal plant
Tripterygium wilfordii
Hook F.</abstract><cop>England</cop><pub>Royal Society of Chemistry</pub><pmid>31588349</pmid><doi>10.1039/c9tx00141g</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-6043-7560</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); Royal Society Of Chemistry Journals 2008-; PubMed Central; Alma/SFX Local Collection |
| subjects | Antioxidants Bioactive compounds Bioassays Biocompatibility Carbonyl compounds Carbonyls Catalase Chemistry Cisplatin Comet assay Damage assessment Damage detection DNA damage Enzymatic activity Epithelial cells Genotoxicity Glutathione Glutathione peroxidase Glutathione reductase Herbal medicine Inflammation Kidneys Medicinal plants Oxidative stress Peroxidase Plant extracts Pretreatment Proteins Reductases Reduction Statistical analysis Superoxide dismutase Toxicity Tumors |
| title | Celastrol pretreatment as a therapeutic option against cisplatin-induced nephrotoxicity |
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