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Gastrodin Protects against Ethanol-Induced Liver Injury and Apoptosis in HepG2 Cells and Animal Models of Alcoholic Liver Disease
This study aims to investigate the protective effects of gastrodin (GSTD), a natural compound isolated from the root of Gastrodia elata BL., on ethanol-induced liver injury and apoptosis in HepG2 cells and animal models. For in vitro studies, GSTD was used to pre-treat the cells for 4 h followed by...
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Published in: | Biological & pharmaceutical bulletin 2018/05/01, Vol.41(5), pp.670-679 |
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description | This study aims to investigate the protective effects of gastrodin (GSTD), a natural compound isolated from the root of Gastrodia elata BL., on ethanol-induced liver injury and apoptosis in HepG2 cells and animal models. For in vitro studies, GSTD was used to pre-treat the cells for 4 h followed by 600 mM of ethanol co-administration for 24 h. Alcoholic liver disease (ALD) of Sprague–Dawley (SD) rats was induced by chronic ethanol-feeding plus a single dose (5 g/kg) of acute ethanol administration, GSTD at different doses were co-administered for 8 weeks. For acute liver injury experiment of ICR mice, GSTD (100 mg/kg/d) was pre-treated for 3 d followed by ethanol administration (5 g/kg) for 3 times. The results showed that GSTD protects HepG2 cells from ethanol-induced toxicity, injury, and apoptosis significantly. Co-administered with ethanol, GSTD prevented the loss of mitochondrial membrane potential, reduced the release cytochrome c from mitochondria, and inhibited the activation of caspase-3 in HepG2 cells. In SD rats induced by chronic ethanol-feeding, GSTD significantly restored liver function and ameliorated pathological changes of the liver. In rat liver, GSTD greatly suppressed the activation of caspase-3 and inhibited hepatocellular apoptosis. In ethanol-induced acute liver injury of ICR mice, GSTD reduced liver acetaldehyde and suppressed the up-regulation of alcohol dehydrogenase (ADH) and CYP2E1 significantly. Our results demonstrate that GSTD is efficacious in protecting liver cells from ethanol-induced injury and apoptosis; it may be useful for the development of novel agents for the treatment of ALD in the future. |
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For in vitro studies, GSTD was used to pre-treat the cells for 4 h followed by 600 mM of ethanol co-administration for 24 h. Alcoholic liver disease (ALD) of Sprague–Dawley (SD) rats was induced by chronic ethanol-feeding plus a single dose (5 g/kg) of acute ethanol administration, GSTD at different doses were co-administered for 8 weeks. For acute liver injury experiment of ICR mice, GSTD (100 mg/kg/d) was pre-treated for 3 d followed by ethanol administration (5 g/kg) for 3 times. The results showed that GSTD protects HepG2 cells from ethanol-induced toxicity, injury, and apoptosis significantly. Co-administered with ethanol, GSTD prevented the loss of mitochondrial membrane potential, reduced the release cytochrome c from mitochondria, and inhibited the activation of caspase-3 in HepG2 cells. In SD rats induced by chronic ethanol-feeding, GSTD significantly restored liver function and ameliorated pathological changes of the liver. In rat liver, GSTD greatly suppressed the activation of caspase-3 and inhibited hepatocellular apoptosis. In ethanol-induced acute liver injury of ICR mice, GSTD reduced liver acetaldehyde and suppressed the up-regulation of alcohol dehydrogenase (ADH) and CYP2E1 significantly. Our results demonstrate that GSTD is efficacious in protecting liver cells from ethanol-induced injury and apoptosis; it may be useful for the development of novel agents for the treatment of ALD in the future.</description><identifier>ISSN: 0918-6158</identifier><identifier>EISSN: 1347-5215</identifier><identifier>DOI: 10.1248/bpb.b17-00825</identifier><identifier>PMID: 29709905</identifier><language>eng</language><publisher>Japan: The Pharmaceutical Society of Japan</publisher><subject>Acetaldehyde ; Activation ; Alcohol dehydrogenase ; Alcoholic beverages ; alcoholic liver disease ; Alcohols ; Animal models ; Apoptosis ; Caspase ; Caspase-3 ; Cytochrome c ; cytotoxicity ; Ethanol ; Feeding ; gastrodin ; Hepatocytes ; Liver ; Liver diseases ; Membrane potential ; Mice ; Mitochondria ; mitochondrial apoptotic pathway ; Rats ; Rodents ; Toxicity</subject><ispartof>Biological and Pharmaceutical Bulletin, 2018/05/01, Vol.41(5), pp.670-679</ispartof><rights>2018 The Pharmaceutical Society of Japan</rights><rights>Copyright Japan Science and Technology Agency 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c702t-3444bdc801fbf2f19929a4930a1bb23c21a92d3ad78720a2193795c62389449f3</citedby><cites>FETCH-LOGICAL-c702t-3444bdc801fbf2f19929a4930a1bb23c21a92d3ad78720a2193795c62389449f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29709905$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Yong</creatorcontrib><creatorcontrib>Wang, Can</creatorcontrib><creatorcontrib>Yu, Bin</creatorcontrib><creatorcontrib>Jiang, Jian-Dong</creatorcontrib><creatorcontrib>Kong, Wei-Jia</creatorcontrib><creatorcontrib>Chinese Academy of Medical Sciences and Peking Union Medical College</creatorcontrib><creatorcontrib>aDepartment of Virology</creatorcontrib><creatorcontrib>and (bState Key Laboratory of Bioactive Natural Products and Function</creatorcontrib><creatorcontrib>Institute of Medicinal Biotechnology</creatorcontrib><creatorcontrib>Institute of Materia Medica</creatorcontrib><title>Gastrodin Protects against Ethanol-Induced Liver Injury and Apoptosis in HepG2 Cells and Animal Models of Alcoholic Liver Disease</title><title>Biological & pharmaceutical bulletin</title><addtitle>Biol Pharm Bull</addtitle><description>This study aims to investigate the protective effects of gastrodin (GSTD), a natural compound isolated from the root of Gastrodia elata BL., on ethanol-induced liver injury and apoptosis in HepG2 cells and animal models. For in vitro studies, GSTD was used to pre-treat the cells for 4 h followed by 600 mM of ethanol co-administration for 24 h. Alcoholic liver disease (ALD) of Sprague–Dawley (SD) rats was induced by chronic ethanol-feeding plus a single dose (5 g/kg) of acute ethanol administration, GSTD at different doses were co-administered for 8 weeks. For acute liver injury experiment of ICR mice, GSTD (100 mg/kg/d) was pre-treated for 3 d followed by ethanol administration (5 g/kg) for 3 times. The results showed that GSTD protects HepG2 cells from ethanol-induced toxicity, injury, and apoptosis significantly. Co-administered with ethanol, GSTD prevented the loss of mitochondrial membrane potential, reduced the release cytochrome c from mitochondria, and inhibited the activation of caspase-3 in HepG2 cells. In SD rats induced by chronic ethanol-feeding, GSTD significantly restored liver function and ameliorated pathological changes of the liver. In rat liver, GSTD greatly suppressed the activation of caspase-3 and inhibited hepatocellular apoptosis. In ethanol-induced acute liver injury of ICR mice, GSTD reduced liver acetaldehyde and suppressed the up-regulation of alcohol dehydrogenase (ADH) and CYP2E1 significantly. Our results demonstrate that GSTD is efficacious in protecting liver cells from ethanol-induced injury and apoptosis; it may be useful for the development of novel agents for the treatment of ALD in the future.</description><subject>Acetaldehyde</subject><subject>Activation</subject><subject>Alcohol dehydrogenase</subject><subject>Alcoholic beverages</subject><subject>alcoholic liver disease</subject><subject>Alcohols</subject><subject>Animal models</subject><subject>Apoptosis</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cytochrome c</subject><subject>cytotoxicity</subject><subject>Ethanol</subject><subject>Feeding</subject><subject>gastrodin</subject><subject>Hepatocytes</subject><subject>Liver</subject><subject>Liver diseases</subject><subject>Membrane potential</subject><subject>Mice</subject><subject>Mitochondria</subject><subject>mitochondrial apoptotic pathway</subject><subject>Rats</subject><subject>Rodents</subject><subject>Toxicity</subject><issn>0918-6158</issn><issn>1347-5215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNpdkc-PEyEUx4nRuN3Vo1dD4sXLrPyaAsemrt0mNXrQM2EYZktDYQTGZI_-59Kdbk28vJfwPnzfF74AvMPoFhMmPnVjd9th3iAkSPsCLDBlvGkJbl-CBZJYNEvciitwnfMBIcQRoa_BFZEcSYnaBfiz0bmk2LsAv6dYrCkZ6gftQi7wrux1iL7Zhn4ytoc799smuA2HKT1CHXq4GuNYYnYZ1uv3dtwQuLbe53kY3FF7-DX2tp7EAa68ifvonTkLfXbZ6mzfgFeD9tm-Pfcb8PPL3Y_1fbP7ttmuV7vGVNOloYyxrjcC4aEbyIClJFIzSZHGXUeoIVhL0lPdc8EJ0gRLymVrloQKyZgc6A34OOuOKf6abC7q6LKpdnWwccqKIEqpYEvMK_rhP_QQpxSquxPFJGasxZVqZsqkmHOygxpTfXJ6VBipUzaqZqNqNuopm8q_P6tO3dH2F_o5jApsZqBOndE-Bu-C_bfbZN656GM1gUUVZRi1tRGFlhydSv0NLiUTVWk9Kx1y0Q_2skqn4oy3T8YYVu2pXAxepmavk7KB_gUpFrc0</recordid><startdate>20180501</startdate><enddate>20180501</enddate><creator>Zhang, Yong</creator><creator>Wang, Can</creator><creator>Yu, Bin</creator><creator>Jiang, Jian-Dong</creator><creator>Kong, Wei-Jia</creator><general>The Pharmaceutical Society of Japan</general><general>Pharmaceutical Society of Japan</general><general>Japan Science and Technology Agency</general><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>7X8</scope></search><sort><creationdate>20180501</creationdate><title>Gastrodin Protects against Ethanol-Induced Liver Injury and Apoptosis in HepG2 Cells and Animal Models of Alcoholic Liver Disease</title><author>Zhang, Yong ; Wang, Can ; Yu, Bin ; Jiang, Jian-Dong ; Kong, Wei-Jia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c702t-3444bdc801fbf2f19929a4930a1bb23c21a92d3ad78720a2193795c62389449f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acetaldehyde</topic><topic>Activation</topic><topic>Alcohol dehydrogenase</topic><topic>Alcoholic beverages</topic><topic>alcoholic liver disease</topic><topic>Alcohols</topic><topic>Animal models</topic><topic>Apoptosis</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Cytochrome c</topic><topic>cytotoxicity</topic><topic>Ethanol</topic><topic>Feeding</topic><topic>gastrodin</topic><topic>Hepatocytes</topic><topic>Liver</topic><topic>Liver diseases</topic><topic>Membrane potential</topic><topic>Mice</topic><topic>Mitochondria</topic><topic>mitochondrial apoptotic pathway</topic><topic>Rats</topic><topic>Rodents</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Yong</creatorcontrib><creatorcontrib>Wang, Can</creatorcontrib><creatorcontrib>Yu, Bin</creatorcontrib><creatorcontrib>Jiang, Jian-Dong</creatorcontrib><creatorcontrib>Kong, Wei-Jia</creatorcontrib><creatorcontrib>Chinese Academy of Medical Sciences and Peking Union Medical College</creatorcontrib><creatorcontrib>aDepartment of Virology</creatorcontrib><creatorcontrib>and (bState Key Laboratory of Bioactive Natural Products and Function</creatorcontrib><creatorcontrib>Institute of Medicinal Biotechnology</creatorcontrib><creatorcontrib>Institute of Materia Medica</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biological & pharmaceutical bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Yong</au><au>Wang, Can</au><au>Yu, Bin</au><au>Jiang, Jian-Dong</au><au>Kong, Wei-Jia</au><aucorp>Chinese Academy of Medical Sciences and Peking Union Medical College</aucorp><aucorp>aDepartment of Virology</aucorp><aucorp>and (bState Key Laboratory of Bioactive Natural Products and Function</aucorp><aucorp>Institute of Medicinal Biotechnology</aucorp><aucorp>Institute of Materia Medica</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gastrodin Protects against Ethanol-Induced Liver Injury and Apoptosis in HepG2 Cells and Animal Models of Alcoholic Liver Disease</atitle><jtitle>Biological & pharmaceutical bulletin</jtitle><addtitle>Biol Pharm Bull</addtitle><date>2018-05-01</date><risdate>2018</risdate><volume>41</volume><issue>5</issue><spage>670</spage><epage>679</epage><pages>670-679</pages><issn>0918-6158</issn><eissn>1347-5215</eissn><abstract>This study aims to investigate the protective effects of gastrodin (GSTD), a natural compound isolated from the root of Gastrodia elata BL., on ethanol-induced liver injury and apoptosis in HepG2 cells and animal models. For in vitro studies, GSTD was used to pre-treat the cells for 4 h followed by 600 mM of ethanol co-administration for 24 h. Alcoholic liver disease (ALD) of Sprague–Dawley (SD) rats was induced by chronic ethanol-feeding plus a single dose (5 g/kg) of acute ethanol administration, GSTD at different doses were co-administered for 8 weeks. For acute liver injury experiment of ICR mice, GSTD (100 mg/kg/d) was pre-treated for 3 d followed by ethanol administration (5 g/kg) for 3 times. The results showed that GSTD protects HepG2 cells from ethanol-induced toxicity, injury, and apoptosis significantly. Co-administered with ethanol, GSTD prevented the loss of mitochondrial membrane potential, reduced the release cytochrome c from mitochondria, and inhibited the activation of caspase-3 in HepG2 cells. In SD rats induced by chronic ethanol-feeding, GSTD significantly restored liver function and ameliorated pathological changes of the liver. In rat liver, GSTD greatly suppressed the activation of caspase-3 and inhibited hepatocellular apoptosis. In ethanol-induced acute liver injury of ICR mice, GSTD reduced liver acetaldehyde and suppressed the up-regulation of alcohol dehydrogenase (ADH) and CYP2E1 significantly. Our results demonstrate that GSTD is efficacious in protecting liver cells from ethanol-induced injury and apoptosis; it may be useful for the development of novel agents for the treatment of ALD in the future.</abstract><cop>Japan</cop><pub>The Pharmaceutical Society of Japan</pub><pmid>29709905</pmid><doi>10.1248/bpb.b17-00825</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acetaldehyde Activation Alcohol dehydrogenase Alcoholic beverages alcoholic liver disease Alcohols Animal models Apoptosis Caspase Caspase-3 Cytochrome c cytotoxicity Ethanol Feeding gastrodin Hepatocytes Liver Liver diseases Membrane potential Mice Mitochondria mitochondrial apoptotic pathway Rats Rodents Toxicity |
title | Gastrodin Protects against Ethanol-Induced Liver Injury and Apoptosis in HepG2 Cells and Animal Models of Alcoholic Liver Disease |
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