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Tacolimus Postconditioning Alleviates Apoptotic Cell Death in Rats after Spinal Cord Ischemia-reperfusion Injury via Up-regulating Protein-Serine-Threonine Kinases Phosphorylation
The effects of tacrolimus postconditioning on protein-serine-threonine kinases (Akt) phos- phorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investi- gated. Ninety male SD rats were randomly divided into sham operation group, ischemia-reperfusion group a...
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Published in: | Journal of Huazhong University of Science and Technology. Medical sciences 2013-12, Vol.33 (6), p.852-856 |
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creator | 潘峰 程艳香 祝成亮 陶凤华 李章华 陶海鹰 贺斌 余铃 戢鹏 唐欢 |
description | The effects of tacrolimus postconditioning on protein-serine-threonine kinases (Akt) phos- phorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investi- gated. Ninety male SD rats were randomly divided into sham operation group, ischemia-reperfusion group and tacrolimus postconditioning group. The model of spinal cord ischemia was established by means of catheterization through femoral artery and balloon dilatation. The spinal cord was reperfused 20 min after ischemia via removing saline out of balloon. The corresponding spinal cord segments were excised and determined for Akt activity in spinal cord tissue by using Western blotting at 5, 15, and 60 min after reperfusion respectively. Spinal cord tissue sections were stained immunohistochemically for detection of the phosphorylated Akt expression at 15 min after reperfusion. Flow cytometry was applied to assess apoptosis of neural cells, and dry-wet weights method was employed to measure water content in spinal cord tissue at 24 h after reperfusion. The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in ischemia-reperfusion group at 5, 15, and 60 min after reperfusion (P〈0.05, P〈0.01). The Akt activities reached the peak at 15 min after reperfu- sion in ischemia-reperfusion group and tacrolimus postconditioning group. The percentage of apoptotic cells and water content in spinal cord tissue were significantly reduced (P〈0.01) in tacrolimus postcon- ditioning group as compared with those in ischemia-reperfusion group at 24 h after reperfusion. It is concluded that tacrolimus postconditioning can increase Akt activity in spinal cord tissue of rats, inhibit apoptosis of neural cells as well as tissue edema, and thereby alleviate spinal cord ischemia-reperfusion injury. |
doi_str_mv | 10.1007/s11596-013-1210-z |
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Ninety male SD rats were randomly divided into sham operation group, ischemia-reperfusion group and tacrolimus postconditioning group. The model of spinal cord ischemia was established by means of catheterization through femoral artery and balloon dilatation. The spinal cord was reperfused 20 min after ischemia via removing saline out of balloon. The corresponding spinal cord segments were excised and determined for Akt activity in spinal cord tissue by using Western blotting at 5, 15, and 60 min after reperfusion respectively. Spinal cord tissue sections were stained immunohistochemically for detection of the phosphorylated Akt expression at 15 min after reperfusion. Flow cytometry was applied to assess apoptosis of neural cells, and dry-wet weights method was employed to measure water content in spinal cord tissue at 24 h after reperfusion. The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in ischemia-reperfusion group at 5, 15, and 60 min after reperfusion (P〈0.05, P〈0.01). The Akt activities reached the peak at 15 min after reperfu- sion in ischemia-reperfusion group and tacrolimus postconditioning group. The percentage of apoptotic cells and water content in spinal cord tissue were significantly reduced (P〈0.01) in tacrolimus postcon- ditioning group as compared with those in ischemia-reperfusion group at 24 h after reperfusion. It is concluded that tacrolimus postconditioning can increase Akt activity in spinal cord tissue of rats, inhibit apoptosis of neural cells as well as tissue edema, and thereby alleviate spinal cord ischemia-reperfusion injury.</description><identifier>ISSN: 1672-0733</identifier><identifier>EISSN: 1993-1352</identifier><identifier>DOI: 10.1007/s11596-013-1210-z</identifier><identifier>PMID: 24337847</identifier><language>eng</language><publisher>Heidelberg: Huazhong University of Science and Technology</publisher><subject>Animals ; Apoptosis - drug effects ; Immunosuppressive Agents - pharmacology ; Immunosuppressive Agents - therapeutic use ; Male ; Medicine ; Medicine & Public Health ; Phosphorylation ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury - drug therapy ; Reperfusion Injury - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; SD大鼠 ; Spinal Cord - drug effects ; Spinal Cord - metabolism ; Spinal Cord - pathology ; Spinal Cord Ischemia - drug therapy ; Spinal Cord Ischemia - metabolism ; Tacrolimus - pharmacology ; Tacrolimus - therapeutic use ; Up-Regulation ; 丝氨酸 ; 后处理 ; 磷酸化 ; 神经细胞凋亡 ; 缺血再灌注损伤 ; 苏氨酸 ; 蛋白质</subject><ispartof>Journal of Huazhong University of Science and Technology. Medical sciences, 2013-12, Vol.33 (6), p.852-856</ispartof><rights>Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2013</rights><rights>Copyright © Wanfang Data Co. Ltd. All Rights Reserved.</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-aeee149f049e2b7c6497b149bce682637cdbe9e1c8f223f4d8810511a0e346a93</citedby><cites>FETCH-LOGICAL-c406t-aeee149f049e2b7c6497b149bce682637cdbe9e1c8f223f4d8810511a0e346a93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/85740A/85740A.jpg</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24337847$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>潘峰 程艳香 祝成亮 陶凤华 李章华 陶海鹰 贺斌 余铃 戢鹏 唐欢</creatorcontrib><title>Tacolimus Postconditioning Alleviates Apoptotic Cell Death in Rats after Spinal Cord Ischemia-reperfusion Injury via Up-regulating Protein-Serine-Threonine Kinases Phosphorylation</title><title>Journal of Huazhong University of Science and Technology. Medical sciences</title><addtitle>J. Huazhong Univ. Sci. Technol. [Med. Sci.]</addtitle><addtitle>Journal of Zuazhong University of Science and Technology: Medical Edition</addtitle><description>The effects of tacrolimus postconditioning on protein-serine-threonine kinases (Akt) phos- phorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investi- gated. Ninety male SD rats were randomly divided into sham operation group, ischemia-reperfusion group and tacrolimus postconditioning group. The model of spinal cord ischemia was established by means of catheterization through femoral artery and balloon dilatation. The spinal cord was reperfused 20 min after ischemia via removing saline out of balloon. The corresponding spinal cord segments were excised and determined for Akt activity in spinal cord tissue by using Western blotting at 5, 15, and 60 min after reperfusion respectively. Spinal cord tissue sections were stained immunohistochemically for detection of the phosphorylated Akt expression at 15 min after reperfusion. Flow cytometry was applied to assess apoptosis of neural cells, and dry-wet weights method was employed to measure water content in spinal cord tissue at 24 h after reperfusion. The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in ischemia-reperfusion group at 5, 15, and 60 min after reperfusion (P〈0.05, P〈0.01). The Akt activities reached the peak at 15 min after reperfu- sion in ischemia-reperfusion group and tacrolimus postconditioning group. The percentage of apoptotic cells and water content in spinal cord tissue were significantly reduced (P〈0.01) in tacrolimus postcon- ditioning group as compared with those in ischemia-reperfusion group at 24 h after reperfusion. It is concluded that tacrolimus postconditioning can increase Akt activity in spinal cord tissue of rats, inhibit apoptosis of neural cells as well as tissue edema, and thereby alleviate spinal cord ischemia-reperfusion injury.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Immunosuppressive Agents - pharmacology</subject><subject>Immunosuppressive Agents - therapeutic use</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Phosphorylation</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>SD大鼠</subject><subject>Spinal Cord - drug effects</subject><subject>Spinal Cord - metabolism</subject><subject>Spinal Cord - pathology</subject><subject>Spinal Cord Ischemia - drug therapy</subject><subject>Spinal Cord Ischemia - metabolism</subject><subject>Tacrolimus - pharmacology</subject><subject>Tacrolimus - therapeutic use</subject><subject>Up-Regulation</subject><subject>丝氨酸</subject><subject>后处理</subject><subject>磷酸化</subject><subject>神经细胞凋亡</subject><subject>缺血再灌注损伤</subject><subject>苏氨酸</subject><subject>蛋白质</subject><issn>1672-0733</issn><issn>1993-1352</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNp9kctu1DAUhiMEoqXwAGyQ2SGhgG9jJ8tquI2oxIhO15bjnEw8ZOzUdqDT1-IFcTRD2bHy5fznO5e_KF4S_I5gLN9HQha1KDFhJaEEl_ePinNS1_nFFvRxvgtJSywZOyuexbjDeCEF5U-LM8oZkxWX58XvjTZ-sPsporWPyXjX2mS9s26LLocBflqdIKLL0Y_JJ2vQEoYBfQCdemQd-q5TRLpLEND1aJ0e0NKHFq2i6WFvdRlghNBNMRPRyu2mcECZiG7GHNlOg05znXXwCawrryFYB-WmDzA3AOhrJsZcfd37OPY-HOYE754XTzo9RHhxOi-Km08fN8sv5dW3z6vl5VVpOBap1ABAeN1hXgNtpBG8lk3-aAyIigomTdtADcRUHaWs421VEbwgRGNgXOiaXRRvj9xf2nXabdXOTyHPGFXaHX60d3eNApqXjwUmJKvfHNVj8LcTxKT2Npq8Le3AT1ERLmpKJMYiS8lRaoKPMUCnxmD3OhwUwWp2Vh2dVRmuZmfVfc55dcJPzR7ah4y_VmYBPQpiDrkthH_t_o_6-tRJ7932Nuc9gHk1jyYJ-wOvpL6K</recordid><startdate>20131201</startdate><enddate>20131201</enddate><creator>潘峰 程艳香 祝成亮 陶凤华 李章华 陶海鹰 贺斌 余铃 戢鹏 唐欢</creator><general>Huazhong University of Science and Technology</general><general>Department of Spine Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China%Department of Gynaecology and Obstetrics, Renmin Hospital of Wuhan University, Wuhan 430060, China%Department of Laboratory Medicine, Renmin Hospital of Wuhan University, Wuhan 430060, China</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</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><scope>7X8</scope><scope>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope></search><sort><creationdate>20131201</creationdate><title>Tacolimus Postconditioning Alleviates Apoptotic Cell Death in Rats after Spinal Cord Ischemia-reperfusion Injury via Up-regulating Protein-Serine-Threonine Kinases Phosphorylation</title><author>潘峰 程艳香 祝成亮 陶凤华 李章华 陶海鹰 贺斌 余铃 戢鹏 唐欢</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c406t-aeee149f049e2b7c6497b149bce682637cdbe9e1c8f223f4d8810511a0e346a93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Immunosuppressive Agents - pharmacology</topic><topic>Immunosuppressive Agents - therapeutic use</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Phosphorylation</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Reperfusion Injury - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>SD大鼠</topic><topic>Spinal Cord - drug effects</topic><topic>Spinal Cord - metabolism</topic><topic>Spinal Cord - pathology</topic><topic>Spinal Cord Ischemia - drug therapy</topic><topic>Spinal Cord Ischemia - metabolism</topic><topic>Tacrolimus - pharmacology</topic><topic>Tacrolimus - therapeutic use</topic><topic>Up-Regulation</topic><topic>丝氨酸</topic><topic>后处理</topic><topic>磷酸化</topic><topic>神经细胞凋亡</topic><topic>缺血再灌注损伤</topic><topic>苏氨酸</topic><topic>蛋白质</topic><toplevel>online_resources</toplevel><creatorcontrib>潘峰 程艳香 祝成亮 陶凤华 李章华 陶海鹰 贺斌 余铃 戢鹏 唐欢</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>维普中文期刊数据库</collection><collection>中文科技期刊数据库-医药卫生</collection><collection>中文科技期刊数据库- 镜像站点</collection><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><collection>Wanfang Data Journals - Hong Kong</collection><collection>WANFANG Data Centre</collection><collection>Wanfang Data Journals</collection><collection>万方数据期刊 - 香港版</collection><collection>China Online Journals (COJ)</collection><collection>China Online Journals (COJ)</collection><jtitle>Journal of Huazhong University of Science and Technology. Medical sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>潘峰 程艳香 祝成亮 陶凤华 李章华 陶海鹰 贺斌 余铃 戢鹏 唐欢</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tacolimus Postconditioning Alleviates Apoptotic Cell Death in Rats after Spinal Cord Ischemia-reperfusion Injury via Up-regulating Protein-Serine-Threonine Kinases Phosphorylation</atitle><jtitle>Journal of Huazhong University of Science and Technology. Medical sciences</jtitle><stitle>J. Huazhong Univ. Sci. Technol. [Med. Sci.]</stitle><addtitle>Journal of Zuazhong University of Science and Technology: Medical Edition</addtitle><date>2013-12-01</date><risdate>2013</risdate><volume>33</volume><issue>6</issue><spage>852</spage><epage>856</epage><pages>852-856</pages><issn>1672-0733</issn><eissn>1993-1352</eissn><abstract>The effects of tacrolimus postconditioning on protein-serine-threonine kinases (Akt) phos- phorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investi- gated. Ninety male SD rats were randomly divided into sham operation group, ischemia-reperfusion group and tacrolimus postconditioning group. The model of spinal cord ischemia was established by means of catheterization through femoral artery and balloon dilatation. The spinal cord was reperfused 20 min after ischemia via removing saline out of balloon. The corresponding spinal cord segments were excised and determined for Akt activity in spinal cord tissue by using Western blotting at 5, 15, and 60 min after reperfusion respectively. Spinal cord tissue sections were stained immunohistochemically for detection of the phosphorylated Akt expression at 15 min after reperfusion. Flow cytometry was applied to assess apoptosis of neural cells, and dry-wet weights method was employed to measure water content in spinal cord tissue at 24 h after reperfusion. The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in ischemia-reperfusion group at 5, 15, and 60 min after reperfusion (P〈0.05, P〈0.01). The Akt activities reached the peak at 15 min after reperfu- sion in ischemia-reperfusion group and tacrolimus postconditioning group. The percentage of apoptotic cells and water content in spinal cord tissue were significantly reduced (P〈0.01) in tacrolimus postcon- ditioning group as compared with those in ischemia-reperfusion group at 24 h after reperfusion. It is concluded that tacrolimus postconditioning can increase Akt activity in spinal cord tissue of rats, inhibit apoptosis of neural cells as well as tissue edema, and thereby alleviate spinal cord ischemia-reperfusion injury.</abstract><cop>Heidelberg</cop><pub>Huazhong University of Science and Technology</pub><pmid>24337847</pmid><doi>10.1007/s11596-013-1210-z</doi><tpages>5</tpages></addata></record> |
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subjects | Animals Apoptosis - drug effects Immunosuppressive Agents - pharmacology Immunosuppressive Agents - therapeutic use Male Medicine Medicine & Public Health Phosphorylation Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Rats Rats, Sprague-Dawley Reperfusion Injury - drug therapy Reperfusion Injury - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism SD大鼠 Spinal Cord - drug effects Spinal Cord - metabolism Spinal Cord - pathology Spinal Cord Ischemia - drug therapy Spinal Cord Ischemia - metabolism Tacrolimus - pharmacology Tacrolimus - therapeutic use Up-Regulation 丝氨酸 后处理 磷酸化 神经细胞凋亡 缺血再灌注损伤 苏氨酸 蛋白质 |
title | Tacolimus Postconditioning Alleviates Apoptotic Cell Death in Rats after Spinal Cord Ischemia-reperfusion Injury via Up-regulating Protein-Serine-Threonine Kinases Phosphorylation |
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