Topical application of nitrosonifedipine, a novel radical scavenger, ameliorates ischemic skin flap necrosis in a mouse model
Ischemic skin flap necrosis can occur in random pattern flaps. An excess amount of reactive oxygen species is generated and causes necrosis in the ischemic tissue. Nitrosonifedipine (NO‐NIF) has been demonstrated to possess potent radical scavenging ability. However, there has been no study on the e...
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| Veröffentlicht in: | Wound repair and regeneration 2017-04, Vol.25 (2), p.217-223 |
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| creator | Fukunaga, Yutaka Izawa‐Ishizawa, Yuki Horinouchi, Yuya Sairyo, Eriko Ikeda, Yasumasa Ishizawa, Keisuke Tsuchiya, Koichiro Abe, Yoshiro Hashimoto, Ichiro Tamaki, Toshiaki |
| description | Ischemic skin flap necrosis can occur in random pattern flaps. An excess amount of reactive oxygen species is generated and causes necrosis in the ischemic tissue. Nitrosonifedipine (NO‐NIF) has been demonstrated to possess potent radical scavenging ability. However, there has been no study on the effects of NO‐NIF on ischemic skin flap necrosis. Therefore, they evaluated the potential of NO‐NIF in ameliorating ischemic skin flap necrosis in a mouse model. A random pattern skin flap (1.0 × 3.0 cm) was elevated on the dorsum of C57BL/6 mice. NO‐NIF was administered by topical injection immediately after surgery and every 24 hours thereafter. Flap survival was evaluated on postoperative day 7. Tissue samples from the skin flaps were harvested on postoperative days 1 and 3 to analyze oxidative stress, apoptosis and endothelial dysfunction. The viable area of the flap in the NO‐NIF group was significantly increased (78.30 ± 7.041%) compared with that of the control group (47.77 ± 6.549%, p |
| doi_str_mv | 10.1111/wrr.12510 |
| format | Article |
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An excess amount of reactive oxygen species is generated and causes necrosis in the ischemic tissue. Nitrosonifedipine (NO‐NIF) has been demonstrated to possess potent radical scavenging ability. However, there has been no study on the effects of NO‐NIF on ischemic skin flap necrosis. Therefore, they evaluated the potential of NO‐NIF in ameliorating ischemic skin flap necrosis in a mouse model. A random pattern skin flap (1.0 × 3.0 cm) was elevated on the dorsum of C57BL/6 mice. NO‐NIF was administered by topical injection immediately after surgery and every 24 hours thereafter. Flap survival was evaluated on postoperative day 7. Tissue samples from the skin flaps were harvested on postoperative days 1 and 3 to analyze oxidative stress, apoptosis and endothelial dysfunction. The viable area of the flap in the NO‐NIF group was significantly increased (78.30 ± 7.041%) compared with that of the control group (47.77 ± 6.549%, p < 0.01). NO‐NIF reduced oxidative stress, apoptosis and endothelial dysfunction, which were evidenced by the decrease of malondialdehyde, p22phox protein expression, number of apoptotic cells, phosphorylated p38 MAPK protein expression, and vascular cell adhesion molecule‐1 protein expression while endothelial nitric oxide synthase protein expression was increased. In conclusion, they demonstrated that NO‐NIF ameliorated ischemic skin flap necrosis by reducing oxidative stress, apoptosis, and endothelial dysfunction. NO‐NIF is considered to be a candidate for the treatment of ischemic flap necrosis.</description><identifier>ISSN: 1067-1927</identifier><identifier>EISSN: 1524-475X</identifier><identifier>DOI: 10.1111/wrr.12510</identifier><identifier>PMID: 28090711</identifier><language>eng</language><publisher>United States</publisher><subject>Administration, Topical ; Animals ; Antioxidants - pharmacology ; Blotting, Western ; Disease Models, Animal ; Graft Survival - drug effects ; Ischemia - drug therapy ; Ischemia - pathology ; Male ; Mice ; Mice, Inbred C57BL ; Necrosis - drug therapy ; Necrosis - pathology ; Nifedipine - administration & dosage ; Nifedipine - analogs & derivatives ; Nifedipine - pharmacology ; Nitroso Compounds - administration & dosage ; Nitroso Compounds - pharmacology ; Oxidative Stress - drug effects ; Reactive Oxygen Species ; Surgical Flaps - blood supply ; Surgical Flaps - pathology ; Wound Healing - drug effects</subject><ispartof>Wound repair and regeneration, 2017-04, Vol.25 (2), p.217-223</ispartof><rights>2017 by the Wound Healing Society</rights><rights>2017 by the Wound Healing Society.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4200-384fd917292744c60a96f950366ffda9db5f4ad16dc098410a0030ecbb02dd1a3</citedby><cites>FETCH-LOGICAL-c4200-384fd917292744c60a96f950366ffda9db5f4ad16dc098410a0030ecbb02dd1a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fwrr.12510$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fwrr.12510$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28090711$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fukunaga, Yutaka</creatorcontrib><creatorcontrib>Izawa‐Ishizawa, Yuki</creatorcontrib><creatorcontrib>Horinouchi, Yuya</creatorcontrib><creatorcontrib>Sairyo, Eriko</creatorcontrib><creatorcontrib>Ikeda, Yasumasa</creatorcontrib><creatorcontrib>Ishizawa, Keisuke</creatorcontrib><creatorcontrib>Tsuchiya, Koichiro</creatorcontrib><creatorcontrib>Abe, Yoshiro</creatorcontrib><creatorcontrib>Hashimoto, Ichiro</creatorcontrib><creatorcontrib>Tamaki, Toshiaki</creatorcontrib><title>Topical application of nitrosonifedipine, a novel radical scavenger, ameliorates ischemic skin flap necrosis in a mouse model</title><title>Wound repair and regeneration</title><addtitle>Wound Repair Regen</addtitle><description>Ischemic skin flap necrosis can occur in random pattern flaps. An excess amount of reactive oxygen species is generated and causes necrosis in the ischemic tissue. Nitrosonifedipine (NO‐NIF) has been demonstrated to possess potent radical scavenging ability. However, there has been no study on the effects of NO‐NIF on ischemic skin flap necrosis. Therefore, they evaluated the potential of NO‐NIF in ameliorating ischemic skin flap necrosis in a mouse model. A random pattern skin flap (1.0 × 3.0 cm) was elevated on the dorsum of C57BL/6 mice. NO‐NIF was administered by topical injection immediately after surgery and every 24 hours thereafter. Flap survival was evaluated on postoperative day 7. Tissue samples from the skin flaps were harvested on postoperative days 1 and 3 to analyze oxidative stress, apoptosis and endothelial dysfunction. The viable area of the flap in the NO‐NIF group was significantly increased (78.30 ± 7.041%) compared with that of the control group (47.77 ± 6.549%, p < 0.01). NO‐NIF reduced oxidative stress, apoptosis and endothelial dysfunction, which were evidenced by the decrease of malondialdehyde, p22phox protein expression, number of apoptotic cells, phosphorylated p38 MAPK protein expression, and vascular cell adhesion molecule‐1 protein expression while endothelial nitric oxide synthase protein expression was increased. In conclusion, they demonstrated that NO‐NIF ameliorated ischemic skin flap necrosis by reducing oxidative stress, apoptosis, and endothelial dysfunction. NO‐NIF is considered to be a candidate for the treatment of ischemic flap necrosis.</description><subject>Administration, Topical</subject><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Blotting, Western</subject><subject>Disease Models, Animal</subject><subject>Graft Survival - drug effects</subject><subject>Ischemia - drug therapy</subject><subject>Ischemia - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Necrosis - drug therapy</subject><subject>Necrosis - pathology</subject><subject>Nifedipine - administration & dosage</subject><subject>Nifedipine - analogs & derivatives</subject><subject>Nifedipine - pharmacology</subject><subject>Nitroso Compounds - administration & dosage</subject><subject>Nitroso Compounds - pharmacology</subject><subject>Oxidative Stress - drug effects</subject><subject>Reactive Oxygen Species</subject><subject>Surgical Flaps - blood supply</subject><subject>Surgical Flaps - pathology</subject><subject>Wound Healing - drug effects</subject><issn>1067-1927</issn><issn>1524-475X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtKBDEQRYMovhf-gGSpYGulJ-nHUgZfIAii6K7JJBWNppM2mXFw4b8bZ9SdWSQFdXKouoTsMThm-ZzMYzxmpWCwQjaZKHnBa_G4mmuo6oK1Zb1BtlJ6AQAh2madbJQNtFAztkk-78JglXRUDoPLxdQGT4Oh3k5jSMFbg9oO1uMRldSHd3Q0Sr34kZR8R_-EMbd6dDZEOcVEbVLP2FtF06v11Dg5UI8qy2zu-WzpwyxhvjW6HbJmpEu4-_Nuk_vzs7vxZXF9c3E1Pr0uFC8BilHDjW5ZXeZVOFcVyLYyrYBRVRmjZasnwnCpWaUVtA1nIAFGgGoygVJrJkfb5GDpHWJ4m2Gadn0eE52THvM0HWsqJpjg0GT0cIl-j5wimm6Itpfxo2PQfafd5bS7RdqZ3f_RziY96j_yN94MnCyBuXX48b-pe7i9XSq_AAYRizM</recordid><startdate>201704</startdate><enddate>201704</enddate><creator>Fukunaga, Yutaka</creator><creator>Izawa‐Ishizawa, Yuki</creator><creator>Horinouchi, Yuya</creator><creator>Sairyo, Eriko</creator><creator>Ikeda, Yasumasa</creator><creator>Ishizawa, Keisuke</creator><creator>Tsuchiya, Koichiro</creator><creator>Abe, Yoshiro</creator><creator>Hashimoto, Ichiro</creator><creator>Tamaki, Toshiaki</creator><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>7X8</scope></search><sort><creationdate>201704</creationdate><title>Topical application of nitrosonifedipine, a novel radical scavenger, ameliorates ischemic skin flap necrosis in a mouse model</title><author>Fukunaga, Yutaka ; Izawa‐Ishizawa, Yuki ; Horinouchi, Yuya ; Sairyo, Eriko ; Ikeda, Yasumasa ; Ishizawa, Keisuke ; Tsuchiya, Koichiro ; Abe, Yoshiro ; Hashimoto, Ichiro ; Tamaki, Toshiaki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4200-384fd917292744c60a96f950366ffda9db5f4ad16dc098410a0030ecbb02dd1a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Administration, Topical</topic><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Blotting, Western</topic><topic>Disease Models, Animal</topic><topic>Graft Survival - drug effects</topic><topic>Ischemia - drug therapy</topic><topic>Ischemia - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Necrosis - drug therapy</topic><topic>Necrosis - pathology</topic><topic>Nifedipine - administration & dosage</topic><topic>Nifedipine - analogs & derivatives</topic><topic>Nifedipine - pharmacology</topic><topic>Nitroso Compounds - administration & dosage</topic><topic>Nitroso Compounds - pharmacology</topic><topic>Oxidative Stress - drug effects</topic><topic>Reactive Oxygen Species</topic><topic>Surgical Flaps - blood supply</topic><topic>Surgical Flaps - pathology</topic><topic>Wound Healing - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fukunaga, Yutaka</creatorcontrib><creatorcontrib>Izawa‐Ishizawa, Yuki</creatorcontrib><creatorcontrib>Horinouchi, Yuya</creatorcontrib><creatorcontrib>Sairyo, Eriko</creatorcontrib><creatorcontrib>Ikeda, Yasumasa</creatorcontrib><creatorcontrib>Ishizawa, Keisuke</creatorcontrib><creatorcontrib>Tsuchiya, Koichiro</creatorcontrib><creatorcontrib>Abe, Yoshiro</creatorcontrib><creatorcontrib>Hashimoto, Ichiro</creatorcontrib><creatorcontrib>Tamaki, Toshiaki</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Wound repair and regeneration</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fukunaga, Yutaka</au><au>Izawa‐Ishizawa, Yuki</au><au>Horinouchi, Yuya</au><au>Sairyo, Eriko</au><au>Ikeda, Yasumasa</au><au>Ishizawa, Keisuke</au><au>Tsuchiya, Koichiro</au><au>Abe, Yoshiro</au><au>Hashimoto, Ichiro</au><au>Tamaki, Toshiaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Topical application of nitrosonifedipine, a novel radical scavenger, ameliorates ischemic skin flap necrosis in a mouse model</atitle><jtitle>Wound repair and regeneration</jtitle><addtitle>Wound Repair Regen</addtitle><date>2017-04</date><risdate>2017</risdate><volume>25</volume><issue>2</issue><spage>217</spage><epage>223</epage><pages>217-223</pages><issn>1067-1927</issn><eissn>1524-475X</eissn><abstract>Ischemic skin flap necrosis can occur in random pattern flaps. An excess amount of reactive oxygen species is generated and causes necrosis in the ischemic tissue. Nitrosonifedipine (NO‐NIF) has been demonstrated to possess potent radical scavenging ability. However, there has been no study on the effects of NO‐NIF on ischemic skin flap necrosis. Therefore, they evaluated the potential of NO‐NIF in ameliorating ischemic skin flap necrosis in a mouse model. A random pattern skin flap (1.0 × 3.0 cm) was elevated on the dorsum of C57BL/6 mice. NO‐NIF was administered by topical injection immediately after surgery and every 24 hours thereafter. Flap survival was evaluated on postoperative day 7. Tissue samples from the skin flaps were harvested on postoperative days 1 and 3 to analyze oxidative stress, apoptosis and endothelial dysfunction. The viable area of the flap in the NO‐NIF group was significantly increased (78.30 ± 7.041%) compared with that of the control group (47.77 ± 6.549%, p < 0.01). NO‐NIF reduced oxidative stress, apoptosis and endothelial dysfunction, which were evidenced by the decrease of malondialdehyde, p22phox protein expression, number of apoptotic cells, phosphorylated p38 MAPK protein expression, and vascular cell adhesion molecule‐1 protein expression while endothelial nitric oxide synthase protein expression was increased. In conclusion, they demonstrated that NO‐NIF ameliorated ischemic skin flap necrosis by reducing oxidative stress, apoptosis, and endothelial dysfunction. NO‐NIF is considered to be a candidate for the treatment of ischemic flap necrosis.</abstract><cop>United States</cop><pmid>28090711</pmid><doi>10.1111/wrr.12510</doi><tpages>7</tpages></addata></record> |
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| subjects | Administration, Topical Animals Antioxidants - pharmacology Blotting, Western Disease Models, Animal Graft Survival - drug effects Ischemia - drug therapy Ischemia - pathology Male Mice Mice, Inbred C57BL Necrosis - drug therapy Necrosis - pathology Nifedipine - administration & dosage Nifedipine - analogs & derivatives Nifedipine - pharmacology Nitroso Compounds - administration & dosage Nitroso Compounds - pharmacology Oxidative Stress - drug effects Reactive Oxygen Species Surgical Flaps - blood supply Surgical Flaps - pathology Wound Healing - drug effects |
| title | Topical application of nitrosonifedipine, a novel radical scavenger, ameliorates ischemic skin flap necrosis in a mouse model |
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