Mechanism of alpha-lipoic acid in attenuating kanamycin-induced ototoxicity
In view of the theory that alpha-lipoic acid effectively prevents cochlear cells from injury caused by various factors such as cisplatin and noise, this study examined whether alpha-lipoic acid can prevent kanamycin-induced ototoxicity. To this end, healthy BALB/c mice were injected subcutaneously w...
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| Veröffentlicht in: | Neural regeneration research 2012-12, Vol.7 (35), p.2793-2800 |
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| creator | Wang, Aimei Hou, Ning Bao, Dongyan Liu, Shuangyue Xu, Tao |
| description | In view of the theory that alpha-lipoic acid effectively prevents cochlear cells from injury caused by various factors such as cisplatin and noise, this study examined whether alpha-lipoic acid can prevent kanamycin-induced ototoxicity. To this end, healthy BALB/c mice were injected subcutaneously with alpha-lipoic acid and kanamycin for 14 days. Auditory brainstem response test showed that increased auditory brainstem response threshold shifts caused by kanamycin were significantly inhibited. Immunohistochemical staining and western blot analysis showed that the expression of phosphorylated p38 mitogen-activated protein kinase and phosphorylated c-Jun N-terminal kinase in mouse cochlea was significantly decreased. The experimental findings suggest that phosphorylated p38 and phosphorylated c-Jun N-terminal kinase mediated kanamycin-induced ototoxic injury in BALB/c mice. AIpha-lipoic acid effectively attenuated kanamycin ototoxicity by inhibiting the kanamycin-induced high expression of phosphorylated p38 and phosphorylated c-Jun N-terminal kinase. |
| doi_str_mv | 10.3969/j.issn.1673-5374.2012.35.007 |
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To this end, healthy BALB/c mice were injected subcutaneously with alpha-lipoic acid and kanamycin for 14 days. Auditory brainstem response test showed that increased auditory brainstem response threshold shifts caused by kanamycin were significantly inhibited. Immunohistochemical staining and western blot analysis showed that the expression of phosphorylated p38 mitogen-activated protein kinase and phosphorylated c-Jun N-terminal kinase in mouse cochlea was significantly decreased. The experimental findings suggest that phosphorylated p38 and phosphorylated c-Jun N-terminal kinase mediated kanamycin-induced ototoxic injury in BALB/c mice. AIpha-lipoic acid effectively attenuated kanamycin ototoxicity by inhibiting the kanamycin-induced high expression of phosphorylated p38 and phosphorylated c-Jun N-terminal kinase.</description><identifier>ISSN: 1673-5374</identifier><identifier>EISSN: 1876-7958</identifier><identifier>DOI: 10.3969/j.issn.1673-5374.2012.35.007</identifier><identifier>PMID: 25317129</identifier><language>eng</language><publisher>India: Medknow Publications & Media Pvt. Ltd</publisher><subject>Acids ; Antioxidants ; Apoptosis ; Autonomic Nerve Damage and Neural Regeneration ; c-Jun ; Experiments ; Hair ; Hearing loss ; Kinases ; Laboratory animals ; Lipid peroxidation ; Lipids ; Noise ; Oxidative stress ; p38丝裂原活化蛋白激酶 ; Rodents ; Signal transduction ; Studies ; α-硫辛酸 ; 免疫组化染色 ; 卡那霉素 ; 听性脑干反应 ; 毒性机制 ; 衰减</subject><ispartof>Neural regeneration research, 2012-12, Vol.7 (35), p.2793-2800</ispartof><rights>2012. 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 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-8426d68536cea9dab2aa34471803006ae3fdc814c10653bf34cb2e166588f0873</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/88507X/88507X.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4190861/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4190861/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25317129$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Aimei</creatorcontrib><creatorcontrib>Hou, Ning</creatorcontrib><creatorcontrib>Bao, Dongyan</creatorcontrib><creatorcontrib>Liu, Shuangyue</creatorcontrib><creatorcontrib>Xu, Tao</creatorcontrib><title>Mechanism of alpha-lipoic acid in attenuating kanamycin-induced ototoxicity</title><title>Neural regeneration research</title><addtitle>Neural Regeneration Research</addtitle><description>In view of the theory that alpha-lipoic acid effectively prevents cochlear cells from injury caused by various factors such as cisplatin and noise, this study examined whether alpha-lipoic acid can prevent kanamycin-induced ototoxicity. To this end, healthy BALB/c mice were injected subcutaneously with alpha-lipoic acid and kanamycin for 14 days. Auditory brainstem response test showed that increased auditory brainstem response threshold shifts caused by kanamycin were significantly inhibited. Immunohistochemical staining and western blot analysis showed that the expression of phosphorylated p38 mitogen-activated protein kinase and phosphorylated c-Jun N-terminal kinase in mouse cochlea was significantly decreased. The experimental findings suggest that phosphorylated p38 and phosphorylated c-Jun N-terminal kinase mediated kanamycin-induced ototoxic injury in BALB/c mice. AIpha-lipoic acid effectively attenuated kanamycin ototoxicity by inhibiting the kanamycin-induced high expression of phosphorylated p38 and phosphorylated c-Jun N-terminal kinase.</description><subject>Acids</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Autonomic Nerve Damage and Neural Regeneration</subject><subject>c-Jun</subject><subject>Experiments</subject><subject>Hair</subject><subject>Hearing loss</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Noise</subject><subject>Oxidative stress</subject><subject>p38丝裂原活化蛋白激酶</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Studies</subject><subject>α-硫辛酸</subject><subject>免疫组化染色</subject><subject>卡那霉素</subject><subject>听性脑干反应</subject><subject>毒性机制</subject><subject>衰减</subject><issn>1673-5374</issn><issn>1876-7958</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNpdkV1r1UAQhhdRbK3-BYnohSCJ-53JTUFK_cCKN3q9zNlscjYmu6fZRHv661057UFlLmZgHt55eYeQV4xWotHN26HyKYWK6VqUStSy4pTxSqiK0voBOWVQ67JuFDzM8z1zQp6kNFCqoOHiMTnhSrCa8eaUfP7i7BaDT1MRuwLH3RbL0e-itwVa3xY-FLgsLqy4-NAXPzDgtLc-lD60q3VtEZdcN976Zf-UPOpwTO7ZXT8j399ffrv4WF59_fDp4t1VaSVTSwmS61aDEto6bFrccEQhZc2ACko1OtG1Fpi0jGolNp2QdsMd01oBdBRqcUbOD7q7dTO51rqwzDia3ewnnPcmojf_boLfmj7-NJI1FDTLAm8OAr8wdBh6M8R1Dtmyue3TcJv2g3F_UhUqZ5rp13fn5ni9urSYySfrxhGDi2syTOckQYOUGX35H3pU5gI40AYoz9Tzv_0fjd9_JQMvDoDdxtBf5-CPjJSaM0ZB_AZQ7J1u</recordid><startdate>20121215</startdate><enddate>20121215</enddate><creator>Wang, Aimei</creator><creator>Hou, Ning</creator><creator>Bao, Dongyan</creator><creator>Liu, Shuangyue</creator><creator>Xu, Tao</creator><general>Medknow Publications & Media Pvt. 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Hou, Ning ; Bao, Dongyan ; Liu, Shuangyue ; Xu, Tao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-8426d68536cea9dab2aa34471803006ae3fdc814c10653bf34cb2e166588f0873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acids</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Autonomic Nerve Damage and Neural Regeneration</topic><topic>c-Jun</topic><topic>Experiments</topic><topic>Hair</topic><topic>Hearing loss</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Lipid peroxidation</topic><topic>Lipids</topic><topic>Noise</topic><topic>Oxidative stress</topic><topic>p38丝裂原活化蛋白激酶</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Studies</topic><topic>α-硫辛酸</topic><topic>免疫组化染色</topic><topic>卡那霉素</topic><topic>听性脑干反应</topic><topic>毒性机制</topic><topic>衰减</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Aimei</creatorcontrib><creatorcontrib>Hou, Ning</creatorcontrib><creatorcontrib>Bao, Dongyan</creatorcontrib><creatorcontrib>Liu, Shuangyue</creatorcontrib><creatorcontrib>Xu, Tao</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>中文科技期刊数据库-7.0平台</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>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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</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>ProQuest Psychology</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><jtitle>Neural regeneration research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Aimei</au><au>Hou, Ning</au><au>Bao, Dongyan</au><au>Liu, Shuangyue</au><au>Xu, Tao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanism of alpha-lipoic acid in attenuating kanamycin-induced ototoxicity</atitle><jtitle>Neural regeneration research</jtitle><addtitle>Neural Regeneration Research</addtitle><date>2012-12-15</date><risdate>2012</risdate><volume>7</volume><issue>35</issue><spage>2793</spage><epage>2800</epage><pages>2793-2800</pages><issn>1673-5374</issn><eissn>1876-7958</eissn><abstract>In view of the theory that alpha-lipoic acid effectively prevents cochlear cells from injury caused by various factors such as cisplatin and noise, this study examined whether alpha-lipoic acid can prevent kanamycin-induced ototoxicity. To this end, healthy BALB/c mice were injected subcutaneously with alpha-lipoic acid and kanamycin for 14 days. Auditory brainstem response test showed that increased auditory brainstem response threshold shifts caused by kanamycin were significantly inhibited. Immunohistochemical staining and western blot analysis showed that the expression of phosphorylated p38 mitogen-activated protein kinase and phosphorylated c-Jun N-terminal kinase in mouse cochlea was significantly decreased. The experimental findings suggest that phosphorylated p38 and phosphorylated c-Jun N-terminal kinase mediated kanamycin-induced ototoxic injury in BALB/c mice. AIpha-lipoic acid effectively attenuated kanamycin ototoxicity by inhibiting the kanamycin-induced high expression of phosphorylated p38 and phosphorylated c-Jun N-terminal kinase.</abstract><cop>India</cop><pub>Medknow Publications & Media Pvt. 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| subjects | Acids Antioxidants Apoptosis Autonomic Nerve Damage and Neural Regeneration c-Jun Experiments Hair Hearing loss Kinases Laboratory animals Lipid peroxidation Lipids Noise Oxidative stress p38丝裂原活化蛋白激酶 Rodents Signal transduction Studies α-硫辛酸 免疫组化染色 卡那霉素 听性脑干反应 毒性机制 衰减 |
| title | Mechanism of alpha-lipoic acid in attenuating kanamycin-induced ototoxicity |
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