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Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis
Methylprednisolone markedly reduces autophagy and apoptosis after secondary spinal cord injury. Here, we investigated whether pretreatment of cells with methylprednisolone would protect neuron-like cells from subsequent oxidative damage via suppression of autophagy and apoptosis. Cultured N2 a cells...
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Published in: | Neural regeneration research 2016-05, Vol.11 (5), p.823-828 |
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description | Methylprednisolone markedly reduces autophagy and apoptosis after secondary spinal cord injury. Here, we investigated whether pretreatment of cells with methylprednisolone would protect neuron-like cells from subsequent oxidative damage via suppression of autophagy and apoptosis. Cultured N2 a cells were pretreated with 10 μM methylprednisolone for 30 minutes, then exposed to 100 μM H2O2 for 24 hours. Inverted phase contrast microscope images, MTT assay, flow cytometry and western blot results showed that, compared to cells exposed to 100 μM H2O2 alone, cells pretreated with methylprednisolone had a significantly lower percentage of apoptotic cells, maintained a healthy morphology, and showed downregulation of autophagic protein light chain 3B and Beclin-1 protein expression. These findings indicate that methylprednisolone exerted neuroprotective effects against oxidative damage by suppressing autophagy and apoptosis. |
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Here, we investigated whether pretreatment of cells with methylprednisolone would protect neuron-like cells from subsequent oxidative damage via suppression of autophagy and apoptosis. Cultured N2 a cells were pretreated with 10 μM methylprednisolone for 30 minutes, then exposed to 100 μM H2O2 for 24 hours. Inverted phase contrast microscope images, MTT assay, flow cytometry and western blot results showed that, compared to cells exposed to 100 μM H2O2 alone, cells pretreated with methylprednisolone had a significantly lower percentage of apoptotic cells, maintained a healthy morphology, and showed downregulation of autophagic protein light chain 3B and Beclin-1 protein expression. These findings indicate that methylprednisolone exerted neuroprotective effects against oxidative damage by suppressing autophagy and apoptosis.</description><identifier>ISSN: 1673-5374</identifier><identifier>EISSN: 1876-7958</identifier><identifier>DOI: 10.4103/1673-5374.182711</identifier><identifier>PMID: 27335569</identifier><language>eng</language><publisher>India: Wolters Kluwer - Medknow Publications</publisher><subject>Analysis ; Apoptosis ; Autophagy ; Autophagy (Cytology) ; Cell growth ; Flow cytometry ; Methylprednisolone ; Morphology ; nerve regeneration; spinal cord injury; methylprednisolone; oxidative stress; N2a cells; autophagy; light chain 3B; Beclin-1; apoptosis; neuroprotection; H 2 O 2 ; neural regeneration ; Oxidative stress ; Polyclonal antibodies ; Proteins ; 氧化损伤 ; 甲基强的松龙 ; 相差显微镜 ; 神经保护作用 ; 神经元样细胞 ; 细胞凋亡 ; 自噬 ; 蛋白表达</subject><ispartof>Neural regeneration research, 2016-05, Vol.11 (5), p.823-828</ispartof><rights>COPYRIGHT 2016 Medknow Publications and Media Pvt. Ltd.</rights><rights>2016. This article is published under (http://creativecommons.org/licenses/by-nc-sa/3.0/) (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright © Wanfang Data Co. Ltd. All Rights Reserved.</rights><rights>Copyright: © Neural Regeneration Research 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c679r-3be5a4c0b56ba171fc330be89357b927c08c64105aa5132857227e60df2655413</citedby><cites>FETCH-LOGICAL-c679r-3be5a4c0b56ba171fc330be89357b927c08c64105aa5132857227e60df2655413</cites><orcidid>0000-0002-5446-6717</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/88507X/88507X.jpg</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2382717930/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2382717930?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27335569$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gao, Wei</creatorcontrib><creatorcontrib>Chen, Shu-rui</creatorcontrib><creatorcontrib>Wu, Meng-yao</creatorcontrib><creatorcontrib>Gao, Kai</creatorcontrib><creatorcontrib>Li, Yuan-long</creatorcontrib><creatorcontrib>Wang, Hong-yu</creatorcontrib><creatorcontrib>Li, Chen-yuan</creatorcontrib><creatorcontrib>Li, Hong</creatorcontrib><title>Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis</title><title>Neural regeneration research</title><addtitle>Neural Regeneration Research</addtitle><description>Methylprednisolone markedly reduces autophagy and apoptosis after secondary spinal cord injury. Here, we investigated whether pretreatment of cells with methylprednisolone would protect neuron-like cells from subsequent oxidative damage via suppression of autophagy and apoptosis. Cultured N2 a cells were pretreated with 10 μM methylprednisolone for 30 minutes, then exposed to 100 μM H2O2 for 24 hours. Inverted phase contrast microscope images, MTT assay, flow cytometry and western blot results showed that, compared to cells exposed to 100 μM H2O2 alone, cells pretreated with methylprednisolone had a significantly lower percentage of apoptotic cells, maintained a healthy morphology, and showed downregulation of autophagic protein light chain 3B and Beclin-1 protein expression. These findings indicate that methylprednisolone exerted neuroprotective effects against oxidative damage by suppressing autophagy and apoptosis.</description><subject>Analysis</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Autophagy (Cytology)</subject><subject>Cell growth</subject><subject>Flow cytometry</subject><subject>Methylprednisolone</subject><subject>Morphology</subject><subject>nerve regeneration; spinal cord injury; methylprednisolone; oxidative stress; N2a cells; autophagy; light chain 3B; Beclin-1; apoptosis; neuroprotection; H 2 O 2 ; neural regeneration</subject><subject>Oxidative stress</subject><subject>Polyclonal antibodies</subject><subject>Proteins</subject><subject>氧化损伤</subject><subject>甲基强的松龙</subject><subject>相差显微镜</subject><subject>神经保护作用</subject><subject>神经元样细胞</subject><subject>细胞凋亡</subject><subject>自噬</subject><subject>蛋白表达</subject><issn>1673-5374</issn><issn>1876-7958</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptkstv1DAQxiMEoqVw54QiuCChLH4_LpVKxaNSERcQR8tJJtlss3ZqJ122fz1e9kEXIR9sjb_5jWf8ZdlLjGYMI_oeC0kLTiWbYUUkxo-yU6ykKKTm6nE6769PsmcxLhDiShP6NDshklLOhT7Nfn6Fcb7uhwC166LvvYMcfkEYY-5gCn4IfoRq7O5SuGnSKeblOg_QTr0dO9fmdhr9MLftOreuzu3gh9HHLj7PnjS2j_Bit59lPz59_H75pbj-9vnq8uK6qITUoaAlcMsqVHJRWixxU1GKSlCacllqIiukKpFa5dZyTInikhAJAtUNEZwzTM-yqy239nZhhtAtbVgbbzvzJ-BDa2wYu6oHU3LGQdegiSoZA6pqhKhVmFuM6oRNrPMta5jKJdQVuDHY_gh6fOO6uWn9nWEaMSZFArzbAlbWNda1ZuGn4FL75r6Ni_u4XhggCAvEEaVJ_XZXLvjbCeJoll2soO-tAz9Fg6XWXDBNWZK--Ud6IBO6-XmpKfqram1qt3ONT6-sNlBzwVLzQhCmkmr2H1VaNSy7Kv1_06X4UQLaJlTBxxigOUwEI7Oxodn4zGx8ZrY2TCmvHk7ykLD3XRJ82E3K9yOEeNNPKwgmaW-cXx2Biwdgowg1e8cmyOvdw-betbfJjYdCQijNJCKI_gYDnfdo</recordid><startdate>20160501</startdate><enddate>20160501</enddate><creator>Gao, Wei</creator><creator>Chen, Shu-rui</creator><creator>Wu, Meng-yao</creator><creator>Gao, Kai</creator><creator>Li, Yuan-long</creator><creator>Wang, Hong-yu</creator><creator>Li, Chen-yuan</creator><creator>Li, Hong</creator><general>Wolters Kluwer - Medknow Publications</general><general>Medknow Publications and Media Pvt. 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Chen, Shu-rui ; Wu, Meng-yao ; Gao, Kai ; Li, Yuan-long ; Wang, Hong-yu ; Li, Chen-yuan ; Li, Hong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c679r-3be5a4c0b56ba171fc330be89357b927c08c64105aa5132857227e60df2655413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Analysis</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Autophagy (Cytology)</topic><topic>Cell growth</topic><topic>Flow cytometry</topic><topic>Methylprednisolone</topic><topic>Morphology</topic><topic>nerve regeneration; spinal cord injury; methylprednisolone; oxidative stress; N2a cells; autophagy; light chain 3B; Beclin-1; apoptosis; neuroprotection; H 2 O 2 ; neural regeneration</topic><topic>Oxidative stress</topic><topic>Polyclonal antibodies</topic><topic>Proteins</topic><topic>氧化损伤</topic><topic>甲基强的松龙</topic><topic>相差显微镜</topic><topic>神经保护作用</topic><topic>神经元样细胞</topic><topic>细胞凋亡</topic><topic>自噬</topic><topic>蛋白表达</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gao, Wei</creatorcontrib><creatorcontrib>Chen, Shu-rui</creatorcontrib><creatorcontrib>Wu, Meng-yao</creatorcontrib><creatorcontrib>Gao, Kai</creatorcontrib><creatorcontrib>Li, Yuan-long</creatorcontrib><creatorcontrib>Wang, Hong-yu</creatorcontrib><creatorcontrib>Li, Chen-yuan</creatorcontrib><creatorcontrib>Li, Hong</creatorcontrib><collection>维普_期刊</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>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Psychology Database (Alumni)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Databases</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Psychology Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</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><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Neural regeneration research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gao, Wei</au><au>Chen, Shu-rui</au><au>Wu, Meng-yao</au><au>Gao, Kai</au><au>Li, Yuan-long</au><au>Wang, Hong-yu</au><au>Li, Chen-yuan</au><au>Li, Hong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis</atitle><jtitle>Neural regeneration research</jtitle><addtitle>Neural Regeneration Research</addtitle><date>2016-05-01</date><risdate>2016</risdate><volume>11</volume><issue>5</issue><spage>823</spage><epage>828</epage><pages>823-828</pages><issn>1673-5374</issn><eissn>1876-7958</eissn><abstract>Methylprednisolone markedly reduces autophagy and apoptosis after secondary spinal cord injury. Here, we investigated whether pretreatment of cells with methylprednisolone would protect neuron-like cells from subsequent oxidative damage via suppression of autophagy and apoptosis. Cultured N2 a cells were pretreated with 10 μM methylprednisolone for 30 minutes, then exposed to 100 μM H2O2 for 24 hours. Inverted phase contrast microscope images, MTT assay, flow cytometry and western blot results showed that, compared to cells exposed to 100 μM H2O2 alone, cells pretreated with methylprednisolone had a significantly lower percentage of apoptotic cells, maintained a healthy morphology, and showed downregulation of autophagic protein light chain 3B and Beclin-1 protein expression. These findings indicate that methylprednisolone exerted neuroprotective effects against oxidative damage by suppressing autophagy and apoptosis.</abstract><cop>India</cop><pub>Wolters Kluwer - Medknow Publications</pub><pmid>27335569</pmid><doi>10.4103/1673-5374.182711</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-5446-6717</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Analysis Apoptosis Autophagy Autophagy (Cytology) Cell growth Flow cytometry Methylprednisolone Morphology nerve regeneration spinal cord injury methylprednisolone oxidative stress N2a cells autophagy light chain 3B Beclin-1 apoptosis neuroprotection H 2 O 2 neural regeneration Oxidative stress Polyclonal antibodies Proteins 氧化损伤 甲基强的松龙 相差显微镜 神经保护作用 神经元样细胞 细胞凋亡 自噬 蛋白表达 |
title | Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis |
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