Hwanggunchungyitang Prevents Cadmium-Induced Ototoxicity through Suppression of the Activation of Caspase-9 and Extracellular Signal-Related Kinase in Auditory HEI-OC1 Cells
Hwanggunchungyitang (HGCYT) is a newly designed herbal drug formula for the purpose of treating auditory diseases. A number of heavy metals have been associated with toxic effects to the peripheral or central auditory system. Cadmium (Cd2+) is a heavy metal and a potent carcinogen implicated in tumo...
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| Veröffentlicht in: | Biological & Pharmaceutical Bulletin 2009/02/01, Vol.32(2), pp.213-219 |
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| creator | Kim, Su-Jin Shin, Bong-Gi Choi, In-Young Kim, Dong-Hyun Kim, Min-cheol Myung, Noh-Yil Moon, Phil-Dong Lee, Jeong-Han An, Hyo-Jin Kim, Na-Hyung Lee, Joo-Young So, Hong-seob Park, Rae-Kil Jeong, Hyun-Ja Um, Jae-Young Kim, Hyung-Min Hong, Seung-Heon |
| description | Hwanggunchungyitang (HGCYT) is a newly designed herbal drug formula for the purpose of treating auditory diseases. A number of heavy metals have been associated with toxic effects to the peripheral or central auditory system. Cadmium (Cd2+) is a heavy metal and a potent carcinogen implicated in tumor development through occupational and environmental exposure. However, the auditory effect of Cd2+ is not poorly understood. The purpose of the present study was to investigate whether HGCYT prevent the ototoxic effects induced by Cd2+ in auditory cell line, HEI-OC1. HGCYT inhibited the cell death, reactive oxygen species generation (ROS), activation of caspase-9, and extracellular signal-related kinase (ERK) induced by Cd2+. In addition, we observed that cochlear hair cells in middle turn were damaged by Cd2+. However, HGCYT prevented the destruction of hair cell arrays of the rat primary organ of Corti explants in the presence of Cd2+. These results support the notion that ROS are involved in Cd2+ ototoxicity and suggest HGCYT therapeutic usefulness, against Cd2+-induced activation of caspase-9 and ERK. |
| doi_str_mv | 10.1248/bpb.32.213 |
| format | Article |
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A number of heavy metals have been associated with toxic effects to the peripheral or central auditory system. Cadmium (Cd2+) is a heavy metal and a potent carcinogen implicated in tumor development through occupational and environmental exposure. However, the auditory effect of Cd2+ is not poorly understood. The purpose of the present study was to investigate whether HGCYT prevent the ototoxic effects induced by Cd2+ in auditory cell line, HEI-OC1. HGCYT inhibited the cell death, reactive oxygen species generation (ROS), activation of caspase-9, and extracellular signal-related kinase (ERK) induced by Cd2+. In addition, we observed that cochlear hair cells in middle turn were damaged by Cd2+. However, HGCYT prevented the destruction of hair cell arrays of the rat primary organ of Corti explants in the presence of Cd2+. These results support the notion that ROS are involved in Cd2+ ototoxicity and suggest HGCYT therapeutic usefulness, against Cd2+-induced activation of caspase-9 and ERK.</description><identifier>ISSN: 0918-6158</identifier><identifier>EISSN: 1347-5215</identifier><identifier>DOI: 10.1248/bpb.32.213</identifier><identifier>PMID: 19182378</identifier><language>eng</language><publisher>Japan: The Pharmaceutical Society of Japan</publisher><subject>Animals ; auditory cell ; Blotting, Western ; cadmium ; Cadmium - antagonists & inhibitors ; Cadmium - metabolism ; Cadmium - toxicity ; Caspase 9 - metabolism ; caspase-9 ; Cell Line ; Cell Survival - drug effects ; Drugs, Chinese Herbal - therapeutic use ; Enzyme Activation - drug effects ; Extracellular Signal-Regulated MAP Kinases - metabolism ; extracellular signal-related kinase ; Hair Cells, Auditory - drug effects ; Hair Cells, Auditory - metabolism ; Hair Cells, Auditory - pathology ; Hearing Disorders - chemically induced ; Hearing Disorders - prevention & control ; Humans ; Hwanggunchungyitang ; Indicators and Reagents ; Mice ; Organ Culture Techniques ; Organ of Corti - drug effects ; Organ of Corti - metabolism ; Organ of Corti - pathology ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; Tetrazolium Salts ; Thiazoles</subject><ispartof>Biological and Pharmaceutical Bulletin, 2009/02/01, Vol.32(2), pp.213-219</ispartof><rights>2009 The Pharmaceutical Society of Japan</rights><rights>Copyright Japan Science and Technology Agency 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c691t-b88306e4fa8381114e1ae59182492449cc08ca456e74aa7eb0c59b1b8c007ff83</citedby><cites>FETCH-LOGICAL-c691t-b88306e4fa8381114e1ae59182492449cc08ca456e74aa7eb0c59b1b8c007ff83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19182378$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Su-Jin</creatorcontrib><creatorcontrib>Shin, Bong-Gi</creatorcontrib><creatorcontrib>Choi, In-Young</creatorcontrib><creatorcontrib>Kim, Dong-Hyun</creatorcontrib><creatorcontrib>Kim, Min-cheol</creatorcontrib><creatorcontrib>Myung, Noh-Yil</creatorcontrib><creatorcontrib>Moon, Phil-Dong</creatorcontrib><creatorcontrib>Lee, Jeong-Han</creatorcontrib><creatorcontrib>An, Hyo-Jin</creatorcontrib><creatorcontrib>Kim, Na-Hyung</creatorcontrib><creatorcontrib>Lee, Joo-Young</creatorcontrib><creatorcontrib>So, Hong-seob</creatorcontrib><creatorcontrib>Park, Rae-Kil</creatorcontrib><creatorcontrib>Jeong, Hyun-Ja</creatorcontrib><creatorcontrib>Um, Jae-Young</creatorcontrib><creatorcontrib>Kim, Hyung-Min</creatorcontrib><creatorcontrib>Hong, Seung-Heon</creatorcontrib><creatorcontrib>fDepartment of Oriental Pharmacy</creatorcontrib><creatorcontrib>aVestibuloCochlear Research Center of Wonkwang University</creatorcontrib><creatorcontrib>dAcupuncture and Meridian Science Research Center</creatorcontrib><creatorcontrib>cBiochip Research Center</creatorcontrib><creatorcontrib>bDepartment of Herb Science</creatorcontrib><creatorcontrib>eCollege of Oriental Medicine</creatorcontrib><creatorcontrib>College of Pharmacy</creatorcontrib><creatorcontrib>Wonkwang University</creatorcontrib><creatorcontrib>Kyung Hee University</creatorcontrib><creatorcontrib>Hoseo University</creatorcontrib><creatorcontrib>ShinSung College</creatorcontrib><title>Hwanggunchungyitang Prevents Cadmium-Induced Ototoxicity through Suppression of the Activation of Caspase-9 and Extracellular Signal-Related Kinase in Auditory HEI-OC1 Cells</title><title>Biological & Pharmaceutical Bulletin</title><addtitle>Biol Pharm Bull</addtitle><description>Hwanggunchungyitang (HGCYT) is a newly designed herbal drug formula for the purpose of treating auditory diseases. A number of heavy metals have been associated with toxic effects to the peripheral or central auditory system. Cadmium (Cd2+) is a heavy metal and a potent carcinogen implicated in tumor development through occupational and environmental exposure. However, the auditory effect of Cd2+ is not poorly understood. The purpose of the present study was to investigate whether HGCYT prevent the ototoxic effects induced by Cd2+ in auditory cell line, HEI-OC1. HGCYT inhibited the cell death, reactive oxygen species generation (ROS), activation of caspase-9, and extracellular signal-related kinase (ERK) induced by Cd2+. In addition, we observed that cochlear hair cells in middle turn were damaged by Cd2+. However, HGCYT prevented the destruction of hair cell arrays of the rat primary organ of Corti explants in the presence of Cd2+. These results support the notion that ROS are involved in Cd2+ ototoxicity and suggest HGCYT therapeutic usefulness, against Cd2+-induced activation of caspase-9 and ERK.</description><subject>Animals</subject><subject>auditory cell</subject><subject>Blotting, Western</subject><subject>cadmium</subject><subject>Cadmium - antagonists & inhibitors</subject><subject>Cadmium - metabolism</subject><subject>Cadmium - toxicity</subject><subject>Caspase 9 - metabolism</subject><subject>caspase-9</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Drugs, Chinese Herbal - therapeutic use</subject><subject>Enzyme Activation - drug effects</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>extracellular signal-related kinase</subject><subject>Hair Cells, Auditory - drug effects</subject><subject>Hair Cells, Auditory - metabolism</subject><subject>Hair Cells, Auditory - pathology</subject><subject>Hearing Disorders - chemically induced</subject><subject>Hearing Disorders - prevention & control</subject><subject>Humans</subject><subject>Hwanggunchungyitang</subject><subject>Indicators and Reagents</subject><subject>Mice</subject><subject>Organ Culture Techniques</subject><subject>Organ of Corti - drug effects</subject><subject>Organ of Corti - metabolism</subject><subject>Organ of Corti - pathology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive Oxygen Species</subject><subject>Tetrazolium Salts</subject><subject>Thiazoles</subject><issn>0918-6158</issn><issn>1347-5215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkW2L1DAQx4so3nr6xg8gAcEXQtc8tNv2lSxlz108WPH0dZimaTdLN6l5OG8_lN_RlK53IIEJM_Ob_0wySfKW4CWhWfmpGZslo0tK2LNkQVhWpDkl-fNkgStSpiuSl1fJK-eOGOMCU_YyuSIxQVlRLpI_29-g-z5ocQi6PysfPfTNynupvUM1tCcVTulOt0HIFu298eZBCeXPyB-sCf0B3YVxtNI5ZTQyXQxLtBZe3YO_RGpwIziZVgh0izYP3oKQwxAGsOhO9RqG9LscwEf9r0pHEimN1qFV3tgz2m526b4mqI4l7nXyooPByTeX-zr5ebP5UW_T2_2XXb2-TcWqIj5typLhlcw6KFlJCMkkAZlPb84qmmWVELgUkOUrWWQAhWywyKuGNKWIP9R1JbtOPsy6ozW_gnSen5SbhgYtTXCc4ozmUSiC7_8DjybY-CTHyZQvGGE0Uh9nSljjnJUdH606gT1zgvm0Qh5XyBnlcYURfneRDM1Jtk_oZWcRuJmBmFUCBqMHpeVTY-GKRpnBxClxxTFmFFOOYycc5SdTxRP9KPR5Fjo6D7187ATWKzHIx6FmMxX_y4gDWC41-wu7kcWb</recordid><startdate>20090201</startdate><enddate>20090201</enddate><creator>Kim, Su-Jin</creator><creator>Shin, Bong-Gi</creator><creator>Choi, In-Young</creator><creator>Kim, Dong-Hyun</creator><creator>Kim, Min-cheol</creator><creator>Myung, Noh-Yil</creator><creator>Moon, Phil-Dong</creator><creator>Lee, Jeong-Han</creator><creator>An, Hyo-Jin</creator><creator>Kim, Na-Hyung</creator><creator>Lee, Joo-Young</creator><creator>So, Hong-seob</creator><creator>Park, Rae-Kil</creator><creator>Jeong, Hyun-Ja</creator><creator>Um, Jae-Young</creator><creator>Kim, Hyung-Min</creator><creator>Hong, Seung-Heon</creator><general>The Pharmaceutical Society of Japan</general><general>Pharmaceutical Society of Japan</general><general>Japan Science and Technology Agency</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20090201</creationdate><title>Hwanggunchungyitang Prevents Cadmium-Induced Ototoxicity through Suppression of the Activation of Caspase-9 and Extracellular Signal-Related Kinase in Auditory HEI-OC1 Cells</title><author>Kim, Su-Jin ; Shin, Bong-Gi ; Choi, In-Young ; Kim, Dong-Hyun ; Kim, Min-cheol ; Myung, Noh-Yil ; Moon, Phil-Dong ; Lee, Jeong-Han ; An, Hyo-Jin ; Kim, Na-Hyung ; Lee, Joo-Young ; So, Hong-seob ; Park, Rae-Kil ; Jeong, Hyun-Ja ; Um, Jae-Young ; Kim, Hyung-Min ; Hong, Seung-Heon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c691t-b88306e4fa8381114e1ae59182492449cc08ca456e74aa7eb0c59b1b8c007ff83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>auditory cell</topic><topic>Blotting, Western</topic><topic>cadmium</topic><topic>Cadmium - antagonists & inhibitors</topic><topic>Cadmium - metabolism</topic><topic>Cadmium - toxicity</topic><topic>Caspase 9 - metabolism</topic><topic>caspase-9</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Drugs, Chinese Herbal - therapeutic use</topic><topic>Enzyme Activation - drug effects</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>extracellular signal-related kinase</topic><topic>Hair Cells, Auditory - drug effects</topic><topic>Hair Cells, Auditory - metabolism</topic><topic>Hair Cells, Auditory - pathology</topic><topic>Hearing Disorders - chemically induced</topic><topic>Hearing Disorders - prevention & control</topic><topic>Humans</topic><topic>Hwanggunchungyitang</topic><topic>Indicators and Reagents</topic><topic>Mice</topic><topic>Organ Culture Techniques</topic><topic>Organ of Corti - drug effects</topic><topic>Organ of Corti - metabolism</topic><topic>Organ of Corti - pathology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive Oxygen Species</topic><topic>Tetrazolium Salts</topic><topic>Thiazoles</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Su-Jin</creatorcontrib><creatorcontrib>Shin, Bong-Gi</creatorcontrib><creatorcontrib>Choi, In-Young</creatorcontrib><creatorcontrib>Kim, Dong-Hyun</creatorcontrib><creatorcontrib>Kim, Min-cheol</creatorcontrib><creatorcontrib>Myung, Noh-Yil</creatorcontrib><creatorcontrib>Moon, Phil-Dong</creatorcontrib><creatorcontrib>Lee, 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Bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Su-Jin</au><au>Shin, Bong-Gi</au><au>Choi, In-Young</au><au>Kim, Dong-Hyun</au><au>Kim, Min-cheol</au><au>Myung, Noh-Yil</au><au>Moon, Phil-Dong</au><au>Lee, Jeong-Han</au><au>An, Hyo-Jin</au><au>Kim, Na-Hyung</au><au>Lee, Joo-Young</au><au>So, Hong-seob</au><au>Park, Rae-Kil</au><au>Jeong, Hyun-Ja</au><au>Um, Jae-Young</au><au>Kim, Hyung-Min</au><au>Hong, Seung-Heon</au><aucorp>fDepartment of Oriental Pharmacy</aucorp><aucorp>aVestibuloCochlear Research Center of Wonkwang University</aucorp><aucorp>dAcupuncture and Meridian Science Research Center</aucorp><aucorp>cBiochip Research Center</aucorp><aucorp>bDepartment of Herb Science</aucorp><aucorp>eCollege of Oriental Medicine</aucorp><aucorp>College of Pharmacy</aucorp><aucorp>Wonkwang University</aucorp><aucorp>Kyung Hee University</aucorp><aucorp>Hoseo University</aucorp><aucorp>ShinSung College</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hwanggunchungyitang Prevents Cadmium-Induced Ototoxicity through Suppression of the Activation of Caspase-9 and Extracellular Signal-Related Kinase in Auditory HEI-OC1 Cells</atitle><jtitle>Biological & Pharmaceutical Bulletin</jtitle><addtitle>Biol Pharm Bull</addtitle><date>2009-02-01</date><risdate>2009</risdate><volume>32</volume><issue>2</issue><spage>213</spage><epage>219</epage><pages>213-219</pages><issn>0918-6158</issn><eissn>1347-5215</eissn><abstract>Hwanggunchungyitang (HGCYT) is a newly designed herbal drug formula for the purpose of treating auditory diseases. A number of heavy metals have been associated with toxic effects to the peripheral or central auditory system. Cadmium (Cd2+) is a heavy metal and a potent carcinogen implicated in tumor development through occupational and environmental exposure. However, the auditory effect of Cd2+ is not poorly understood. The purpose of the present study was to investigate whether HGCYT prevent the ototoxic effects induced by Cd2+ in auditory cell line, HEI-OC1. HGCYT inhibited the cell death, reactive oxygen species generation (ROS), activation of caspase-9, and extracellular signal-related kinase (ERK) induced by Cd2+. In addition, we observed that cochlear hair cells in middle turn were damaged by Cd2+. However, HGCYT prevented the destruction of hair cell arrays of the rat primary organ of Corti explants in the presence of Cd2+. These results support the notion that ROS are involved in Cd2+ ototoxicity and suggest HGCYT therapeutic usefulness, against Cd2+-induced activation of caspase-9 and ERK.</abstract><cop>Japan</cop><pub>The Pharmaceutical Society of Japan</pub><pmid>19182378</pmid><doi>10.1248/bpb.32.213</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0918-6158 |
| ispartof | Biological and Pharmaceutical Bulletin, 2009/02/01, Vol.32(2), pp.213-219 |
| issn | 0918-6158 1347-5215 |
| language | eng |
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| source | J-STAGE Free; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Free Full-Text Journals in Chemistry |
| subjects | Animals auditory cell Blotting, Western cadmium Cadmium - antagonists & inhibitors Cadmium - metabolism Cadmium - toxicity Caspase 9 - metabolism caspase-9 Cell Line Cell Survival - drug effects Drugs, Chinese Herbal - therapeutic use Enzyme Activation - drug effects Extracellular Signal-Regulated MAP Kinases - metabolism extracellular signal-related kinase Hair Cells, Auditory - drug effects Hair Cells, Auditory - metabolism Hair Cells, Auditory - pathology Hearing Disorders - chemically induced Hearing Disorders - prevention & control Humans Hwanggunchungyitang Indicators and Reagents Mice Organ Culture Techniques Organ of Corti - drug effects Organ of Corti - metabolism Organ of Corti - pathology Rats Rats, Sprague-Dawley Reactive Oxygen Species Tetrazolium Salts Thiazoles |
| title | Hwanggunchungyitang Prevents Cadmium-Induced Ototoxicity through Suppression of the Activation of Caspase-9 and Extracellular Signal-Related Kinase in Auditory HEI-OC1 Cells |
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