Selenium Ameliorate Peripheral Nerve Ischemic-Reperfusion Injury via Decreased TNF-α
Selenium is considered as a trace element that plays antioxidant role in the body. So, the aim of this study was to evaluate the effect of selenium on ameliorating of sciatic nerve ischemia-reperfusion injury. Eighty (80) adult male Wistar rats weighing 250–300 g were used. They were divided into 10...
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Veröffentlicht in: | Biological trace element research 2017-04, Vol.176 (2), p.328-337 |
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creator | Zendedel, Abolfazl Gharibi, Zahra Anbari, Khatereh Abbaszadeh, Abolfazl khayat, Zahra Khanipour Khorramabadi, Reza Mohammadrezaei Soleymaninejad, Maryam Gholami, Mohammadreza |
description | Selenium is considered as a trace element that plays antioxidant role in the body. So, the aim of this study was to evaluate the effect of selenium on ameliorating of sciatic nerve ischemia-reperfusion injury. Eighty (80) adult male Wistar rats weighing 250–300 g were used. They were divided into 10 groups (
n
= 8). Then, femoral vessels were obstructed by using 4/0 silk and splitknot techniques. After 3-h ischemia for all the groups, reperfusion was applied for different periods: 3, 7, 14, and 28 days. In half of each experimental group, 0.2 mg/kg selenium was injected intraperitoneally, coinciding with ischemia. After reperfusion, according to the grouping, rats were killed by using high dose of anesthetic drug and then sciatic nerve was removed and fixed. Then, tissue samples were processed and subsequently stained with hematoxylin-eosin, apoptosis, and immunohistochemistry stains. On the third day of reperfusion, the amount of TNF-α as an inflammatory marker of ischemia-reperfusion acute phase increased. On the seventh day of reperfusion, the amount of NF-кB as an apoptotic index and infiltration of mast cells increased in the tissue as a result of development of inflammation. But, on the 14th day of reperfusion, the amount of NF-кB as an apoptotic index decreased to the lowest amount. On the 28th day of reperfusion, the amount of TNF-α as an inflammatory marker decreased to its lowest level. Prescription of selenium concurrent with development of ischemia can reduce the damage caused by sciatic nerve ischemia-reperfusion. |
doi_str_mv | 10.1007/s12011-016-0836-7 |
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n
= 8). Then, femoral vessels were obstructed by using 4/0 silk and splitknot techniques. After 3-h ischemia for all the groups, reperfusion was applied for different periods: 3, 7, 14, and 28 days. In half of each experimental group, 0.2 mg/kg selenium was injected intraperitoneally, coinciding with ischemia. After reperfusion, according to the grouping, rats were killed by using high dose of anesthetic drug and then sciatic nerve was removed and fixed. Then, tissue samples were processed and subsequently stained with hematoxylin-eosin, apoptosis, and immunohistochemistry stains. On the third day of reperfusion, the amount of TNF-α as an inflammatory marker of ischemia-reperfusion acute phase increased. On the seventh day of reperfusion, the amount of NF-кB as an apoptotic index and infiltration of mast cells increased in the tissue as a result of development of inflammation. But, on the 14th day of reperfusion, the amount of NF-кB as an apoptotic index decreased to the lowest amount. On the 28th day of reperfusion, the amount of TNF-α as an inflammatory marker decreased to its lowest level. Prescription of selenium concurrent with development of ischemia can reduce the damage caused by sciatic nerve ischemia-reperfusion.</description><identifier>ISSN: 0163-4984</identifier><identifier>EISSN: 1559-0720</identifier><identifier>DOI: 10.1007/s12011-016-0836-7</identifier><identifier>PMID: 27600929</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Biochemistry ; Biomedical and Life Sciences ; Biotechnology ; Disease Models, Animal ; Injections, Intraperitoneal ; Ischemia - drug therapy ; Ischemia - metabolism ; Ischemia - pathology ; Life Sciences ; Male ; Nutrition ; Oncology ; Peripheral Nerves - drug effects ; Peripheral Nerves - metabolism ; Peripheral Nerves - pathology ; Rats ; Rats, Wistar ; Reperfusion Injury - drug therapy ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Selenium - administration & dosage ; Selenium - pharmacology ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Biological trace element research, 2017-04, Vol.176 (2), p.328-337</ispartof><rights>Springer Science+Business Media New York 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c377t-9b85ba713219c5ecf20a671fd26aef8c1f2e03b73d94efb2afe5d1d3e25dac5b3</citedby><cites>FETCH-LOGICAL-c377t-9b85ba713219c5ecf20a671fd26aef8c1f2e03b73d94efb2afe5d1d3e25dac5b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12011-016-0836-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12011-016-0836-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27600929$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zendedel, Abolfazl</creatorcontrib><creatorcontrib>Gharibi, Zahra</creatorcontrib><creatorcontrib>Anbari, Khatereh</creatorcontrib><creatorcontrib>Abbaszadeh, Abolfazl</creatorcontrib><creatorcontrib>khayat, Zahra Khanipour</creatorcontrib><creatorcontrib>Khorramabadi, Reza Mohammadrezaei</creatorcontrib><creatorcontrib>Soleymaninejad, Maryam</creatorcontrib><creatorcontrib>Gholami, Mohammadreza</creatorcontrib><title>Selenium Ameliorate Peripheral Nerve Ischemic-Reperfusion Injury via Decreased TNF-α</title><title>Biological trace element research</title><addtitle>Biol Trace Elem Res</addtitle><addtitle>Biol Trace Elem Res</addtitle><description>Selenium is considered as a trace element that plays antioxidant role in the body. So, the aim of this study was to evaluate the effect of selenium on ameliorating of sciatic nerve ischemia-reperfusion injury. Eighty (80) adult male Wistar rats weighing 250–300 g were used. They were divided into 10 groups (
n
= 8). Then, femoral vessels were obstructed by using 4/0 silk and splitknot techniques. After 3-h ischemia for all the groups, reperfusion was applied for different periods: 3, 7, 14, and 28 days. In half of each experimental group, 0.2 mg/kg selenium was injected intraperitoneally, coinciding with ischemia. After reperfusion, according to the grouping, rats were killed by using high dose of anesthetic drug and then sciatic nerve was removed and fixed. Then, tissue samples were processed and subsequently stained with hematoxylin-eosin, apoptosis, and immunohistochemistry stains. On the third day of reperfusion, the amount of TNF-α as an inflammatory marker of ischemia-reperfusion acute phase increased. On the seventh day of reperfusion, the amount of NF-кB as an apoptotic index and infiltration of mast cells increased in the tissue as a result of development of inflammation. But, on the 14th day of reperfusion, the amount of NF-кB as an apoptotic index decreased to the lowest amount. On the 28th day of reperfusion, the amount of TNF-α as an inflammatory marker decreased to its lowest level. Prescription of selenium concurrent with development of ischemia can reduce the damage caused by sciatic nerve ischemia-reperfusion.</description><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biotechnology</subject><subject>Disease Models, Animal</subject><subject>Injections, Intraperitoneal</subject><subject>Ischemia - drug therapy</subject><subject>Ischemia - metabolism</subject><subject>Ischemia - pathology</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Nutrition</subject><subject>Oncology</subject><subject>Peripheral Nerves - drug effects</subject><subject>Peripheral Nerves - metabolism</subject><subject>Peripheral Nerves - pathology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Selenium - administration & dosage</subject><subject>Selenium - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0163-4984</issn><issn>1559-0720</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkLtOwzAYhS0EoqXwACwoI4vBlySOx6pQqIQKgna2HOc3TZUbdlOpj8WL8EykSmFETGc43znDh9AlJTeUEHHrKSOUYkJjTBIeY3GEhjSKJCaCkWM07AqOQ5mEA3Tm_ZoQKpjkp2jAREyIZHKIlm9QQJW3ZTAuochrpzcQvIDLmxU4XQRzcFsIZt6soMwNfoUGnG19XlfBrFq3bhdscx3cgXGgPWTBYj7FX5_n6MTqwsPFIUdoOb1fTB7x0_PDbDJ-woYLscEyTaJUC8oZlSYCYxnRsaA2Y7EGmxhqGRCeCp7JEGzKtIUooxkHFmXaRCkfoev-t3H1Rwt-o8rcGygKXUHdekWTJJExi0X8DzSSnTUeJh1Ke9S42nsHVjUuL7XbKUrUXrzqxavOr9qLV6LbXB3u27SE7HfxY7oDWA_4rqrewal13bqqs_PH6zd1VI8A</recordid><startdate>20170401</startdate><enddate>20170401</enddate><creator>Zendedel, Abolfazl</creator><creator>Gharibi, Zahra</creator><creator>Anbari, Khatereh</creator><creator>Abbaszadeh, Abolfazl</creator><creator>khayat, Zahra Khanipour</creator><creator>Khorramabadi, Reza Mohammadrezaei</creator><creator>Soleymaninejad, Maryam</creator><creator>Gholami, Mohammadreza</creator><general>Springer US</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>7X8</scope><scope>7TK</scope></search><sort><creationdate>20170401</creationdate><title>Selenium Ameliorate Peripheral Nerve Ischemic-Reperfusion Injury via Decreased TNF-α</title><author>Zendedel, Abolfazl ; Gharibi, Zahra ; Anbari, Khatereh ; Abbaszadeh, Abolfazl ; khayat, Zahra Khanipour ; Khorramabadi, Reza Mohammadrezaei ; Soleymaninejad, Maryam ; Gholami, Mohammadreza</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c377t-9b85ba713219c5ecf20a671fd26aef8c1f2e03b73d94efb2afe5d1d3e25dac5b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biotechnology</topic><topic>Disease Models, Animal</topic><topic>Injections, Intraperitoneal</topic><topic>Ischemia - drug therapy</topic><topic>Ischemia - metabolism</topic><topic>Ischemia - pathology</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Nutrition</topic><topic>Oncology</topic><topic>Peripheral Nerves - drug effects</topic><topic>Peripheral Nerves - metabolism</topic><topic>Peripheral Nerves - pathology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Selenium - administration & dosage</topic><topic>Selenium - pharmacology</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zendedel, Abolfazl</creatorcontrib><creatorcontrib>Gharibi, Zahra</creatorcontrib><creatorcontrib>Anbari, Khatereh</creatorcontrib><creatorcontrib>Abbaszadeh, Abolfazl</creatorcontrib><creatorcontrib>khayat, Zahra Khanipour</creatorcontrib><creatorcontrib>Khorramabadi, Reza Mohammadrezaei</creatorcontrib><creatorcontrib>Soleymaninejad, Maryam</creatorcontrib><creatorcontrib>Gholami, Mohammadreza</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><collection>Neurosciences Abstracts</collection><jtitle>Biological trace element research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zendedel, Abolfazl</au><au>Gharibi, Zahra</au><au>Anbari, Khatereh</au><au>Abbaszadeh, Abolfazl</au><au>khayat, Zahra Khanipour</au><au>Khorramabadi, Reza Mohammadrezaei</au><au>Soleymaninejad, Maryam</au><au>Gholami, Mohammadreza</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Selenium Ameliorate Peripheral Nerve Ischemic-Reperfusion Injury via Decreased TNF-α</atitle><jtitle>Biological trace element research</jtitle><stitle>Biol Trace Elem Res</stitle><addtitle>Biol Trace Elem Res</addtitle><date>2017-04-01</date><risdate>2017</risdate><volume>176</volume><issue>2</issue><spage>328</spage><epage>337</epage><pages>328-337</pages><issn>0163-4984</issn><eissn>1559-0720</eissn><abstract>Selenium is considered as a trace element that plays antioxidant role in the body. So, the aim of this study was to evaluate the effect of selenium on ameliorating of sciatic nerve ischemia-reperfusion injury. Eighty (80) adult male Wistar rats weighing 250–300 g were used. They were divided into 10 groups (
n
= 8). Then, femoral vessels were obstructed by using 4/0 silk and splitknot techniques. After 3-h ischemia for all the groups, reperfusion was applied for different periods: 3, 7, 14, and 28 days. In half of each experimental group, 0.2 mg/kg selenium was injected intraperitoneally, coinciding with ischemia. After reperfusion, according to the grouping, rats were killed by using high dose of anesthetic drug and then sciatic nerve was removed and fixed. Then, tissue samples were processed and subsequently stained with hematoxylin-eosin, apoptosis, and immunohistochemistry stains. On the third day of reperfusion, the amount of TNF-α as an inflammatory marker of ischemia-reperfusion acute phase increased. On the seventh day of reperfusion, the amount of NF-кB as an apoptotic index and infiltration of mast cells increased in the tissue as a result of development of inflammation. But, on the 14th day of reperfusion, the amount of NF-кB as an apoptotic index decreased to the lowest amount. On the 28th day of reperfusion, the amount of TNF-α as an inflammatory marker decreased to its lowest level. Prescription of selenium concurrent with development of ischemia can reduce the damage caused by sciatic nerve ischemia-reperfusion.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>27600929</pmid><doi>10.1007/s12011-016-0836-7</doi><tpages>10</tpages></addata></record> |
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subjects | Animals Biochemistry Biomedical and Life Sciences Biotechnology Disease Models, Animal Injections, Intraperitoneal Ischemia - drug therapy Ischemia - metabolism Ischemia - pathology Life Sciences Male Nutrition Oncology Peripheral Nerves - drug effects Peripheral Nerves - metabolism Peripheral Nerves - pathology Rats Rats, Wistar Reperfusion Injury - drug therapy Reperfusion Injury - metabolism Reperfusion Injury - pathology Selenium - administration & dosage Selenium - pharmacology Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - metabolism |
title | Selenium Ameliorate Peripheral Nerve Ischemic-Reperfusion Injury via Decreased TNF-α |
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