1O, 20O-diacetyl kamebakaurin protects against acetaminophen-induced hepatotoxicity in mice
The present study aimed to investigate the protective effects of kamebakaurin (KA) and 1O, 20O-diacetyl kamebakaurin (Ac2KA) on acetaminophen (APAP)-induced hepatotoxicity and compare the hepatoprotective mechanisms of the two chemicals. Seven-week-old male C57BL/6J mice were orally administered KA,...
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| Veröffentlicht in: | Biomedical Research 2018/10/01, Vol.39(5), pp.251-260 |
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| creator | YOSHIOKA, Hiroki NONOGAKI, Tsunemasa OHNISHI, Hiroyuki FUKUISHI, Nobuyuki YOSHIKAWA, Masae GUI, Ming-Yu JIN, Yong-Ri LI, Xu-Wen ADACHI, Yoshiyuki OHNO, Naohito TAKEYA, Koichi HITOTSUYANAGI, Yukio MIURA, Nobuhiko AOYAGI, Yutaka |
| description | The present study aimed to investigate the protective effects of kamebakaurin (KA) and 1O, 20O-diacetyl kamebakaurin (Ac2KA) on acetaminophen (APAP)-induced hepatotoxicity and compare the hepatoprotective mechanisms of the two chemicals. Seven-week-old male C57BL/6J mice were orally administered KA, Ac2KA, or an ethanol/olive oil emulsion once per day for 7-days. Twenty-four hours after the final administration, the mice were fasted and then intraperitoneally injected with 450 mg/kg APAP or saline. At 16 h after injection, the mice were euthanized and blood samples were collected for plasma analysis. Pretreatment with KA and Ac2KA significantly attenuated APAP-induced hepatic injury. The protective effect of Ac2KA was stronger than that of KA. These two chemicals attenuated oxidative stress, inflammatory cytokine production, c-jun N-terminal kinase activation, and receptor-interacting protein (RIP)-3 activation. Ac2KA also decreased APAP-induced RIP-1 activation and nuclear factor kappa B (NF-κB) p65 translocation. Moreover, Ac2KA repressed mRNA expression of Cyp1a2/2e1 in the liver. Our results showed that KA and Ac2KA exerted protective effects against APAP-induced hepatotoxicity. The responsible mechanisms may be related to the chemicals’ antioxidant activity and the inhibition of c-jun N-terminal kinase activation and RIP-3 activation. The effects of Ac2KA included those of KA, as well as RIP-1 inactivation, NF-κB inhibition, and Cyp inhibition. |
| doi_str_mv | 10.2220/biomedres.39.251 |
| format | Article |
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Seven-week-old male C57BL/6J mice were orally administered KA, Ac2KA, or an ethanol/olive oil emulsion once per day for 7-days. Twenty-four hours after the final administration, the mice were fasted and then intraperitoneally injected with 450 mg/kg APAP or saline. At 16 h after injection, the mice were euthanized and blood samples were collected for plasma analysis. Pretreatment with KA and Ac2KA significantly attenuated APAP-induced hepatic injury. The protective effect of Ac2KA was stronger than that of KA. These two chemicals attenuated oxidative stress, inflammatory cytokine production, c-jun N-terminal kinase activation, and receptor-interacting protein (RIP)-3 activation. Ac2KA also decreased APAP-induced RIP-1 activation and nuclear factor kappa B (NF-κB) p65 translocation. Moreover, Ac2KA repressed mRNA expression of Cyp1a2/2e1 in the liver. Our results showed that KA and Ac2KA exerted protective effects against APAP-induced hepatotoxicity. The responsible mechanisms may be related to the chemicals’ antioxidant activity and the inhibition of c-jun N-terminal kinase activation and RIP-3 activation. The effects of Ac2KA included those of KA, as well as RIP-1 inactivation, NF-κB inhibition, and Cyp inhibition.</description><identifier>ISSN: 0388-6107</identifier><identifier>EISSN: 1880-313X</identifier><identifier>DOI: 10.2220/biomedres.39.251</identifier><identifier>PMID: 30333432</identifier><language>eng</language><publisher>Japan: Biomedical Research Press</publisher><subject>Acetaminophen ; Acetaminophen - adverse effects ; Activation ; Analgesics ; Animals ; Antioxidants ; Antioxidants - chemistry ; Antioxidants - pharmacology ; Biomarkers ; c-Jun protein ; Chemical activity ; Chemical and Drug Induced Liver Injury - drug therapy ; Chemical and Drug Induced Liver Injury - metabolism ; Chemical and Drug Induced Liver Injury - pathology ; Chemicals ; CYP1A2 protein ; Cytochrome P450 ; Cytokines - metabolism ; Deactivation ; Diacetyl ; Disease Models, Animal ; Diterpenes - chemistry ; Diterpenes - pharmacology ; Ethanol ; Gene expression ; Glutathione - metabolism ; Hepatotoxicity ; Inactivation ; Inflammation ; Inflammation Mediators - metabolism ; Inhibition ; Injury analysis ; JNK protein ; Kinases ; Liver ; Liver Function Tests ; Male ; Malondialdehyde - metabolism ; Mice ; Molecular Structure ; NF-κB protein ; Oils & fats ; Olive oil ; Oral administration ; Organic chemistry ; Oxidative stress ; Oxidative Stress - drug effects ; Protective Agents - chemistry ; Protective Agents - pharmacology ; Protein Transport ; Reactive Oxygen Species - metabolism ; Transcription factors ; Translocation</subject><ispartof>Biomedical Research, 2018/10/01, Vol.39(5), pp.251-260</ispartof><rights>2018 Biomedical Research Press</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-c560t-dd9d0fe0c00396d3885568572d9911529338d8b5bb87d6e3962f2ca648d8da3a3</citedby><cites>FETCH-LOGICAL-c560t-dd9d0fe0c00396d3885568572d9911529338d8b5bb87d6e3962f2ca648d8da3a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30333432$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>YOSHIOKA, Hiroki</creatorcontrib><creatorcontrib>NONOGAKI, Tsunemasa</creatorcontrib><creatorcontrib>OHNISHI, Hiroyuki</creatorcontrib><creatorcontrib>FUKUISHI, Nobuyuki</creatorcontrib><creatorcontrib>YOSHIKAWA, Masae</creatorcontrib><creatorcontrib>GUI, Ming-Yu</creatorcontrib><creatorcontrib>JIN, Yong-Ri</creatorcontrib><creatorcontrib>LI, Xu-Wen</creatorcontrib><creatorcontrib>ADACHI, Yoshiyuki</creatorcontrib><creatorcontrib>OHNO, Naohito</creatorcontrib><creatorcontrib>TAKEYA, Koichi</creatorcontrib><creatorcontrib>HITOTSUYANAGI, Yukio</creatorcontrib><creatorcontrib>MIURA, Nobuhiko</creatorcontrib><creatorcontrib>AOYAGI, Yutaka</creatorcontrib><title>1O, 20O-diacetyl kamebakaurin protects against acetaminophen-induced hepatotoxicity in mice</title><title>Biomedical Research</title><addtitle>Biomed. Res.</addtitle><description>The present study aimed to investigate the protective effects of kamebakaurin (KA) and 1O, 20O-diacetyl kamebakaurin (Ac2KA) on acetaminophen (APAP)-induced hepatotoxicity and compare the hepatoprotective mechanisms of the two chemicals. Seven-week-old male C57BL/6J mice were orally administered KA, Ac2KA, or an ethanol/olive oil emulsion once per day for 7-days. Twenty-four hours after the final administration, the mice were fasted and then intraperitoneally injected with 450 mg/kg APAP or saline. At 16 h after injection, the mice were euthanized and blood samples were collected for plasma analysis. Pretreatment with KA and Ac2KA significantly attenuated APAP-induced hepatic injury. The protective effect of Ac2KA was stronger than that of KA. These two chemicals attenuated oxidative stress, inflammatory cytokine production, c-jun N-terminal kinase activation, and receptor-interacting protein (RIP)-3 activation. Ac2KA also decreased APAP-induced RIP-1 activation and nuclear factor kappa B (NF-κB) p65 translocation. Moreover, Ac2KA repressed mRNA expression of Cyp1a2/2e1 in the liver. Our results showed that KA and Ac2KA exerted protective effects against APAP-induced hepatotoxicity. The responsible mechanisms may be related to the chemicals’ antioxidant activity and the inhibition of c-jun N-terminal kinase activation and RIP-3 activation. The effects of Ac2KA included those of KA, as well as RIP-1 inactivation, NF-κB inhibition, and Cyp inhibition.</description><subject>Acetaminophen</subject><subject>Acetaminophen - adverse effects</subject><subject>Activation</subject><subject>Analgesics</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - chemistry</subject><subject>Antioxidants - pharmacology</subject><subject>Biomarkers</subject><subject>c-Jun protein</subject><subject>Chemical activity</subject><subject>Chemical and Drug Induced Liver Injury - drug therapy</subject><subject>Chemical and Drug Induced Liver Injury - metabolism</subject><subject>Chemical and Drug Induced Liver Injury - pathology</subject><subject>Chemicals</subject><subject>CYP1A2 protein</subject><subject>Cytochrome P450</subject><subject>Cytokines - metabolism</subject><subject>Deactivation</subject><subject>Diacetyl</subject><subject>Disease Models, Animal</subject><subject>Diterpenes - chemistry</subject><subject>Diterpenes - pharmacology</subject><subject>Ethanol</subject><subject>Gene expression</subject><subject>Glutathione - metabolism</subject><subject>Hepatotoxicity</subject><subject>Inactivation</subject><subject>Inflammation</subject><subject>Inflammation Mediators - metabolism</subject><subject>Inhibition</subject><subject>Injury analysis</subject><subject>JNK protein</subject><subject>Kinases</subject><subject>Liver</subject><subject>Liver Function Tests</subject><subject>Male</subject><subject>Malondialdehyde - metabolism</subject><subject>Mice</subject><subject>Molecular Structure</subject><subject>NF-κB protein</subject><subject>Oils & fats</subject><subject>Olive oil</subject><subject>Oral administration</subject><subject>Organic chemistry</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Protective Agents - chemistry</subject><subject>Protective Agents - pharmacology</subject><subject>Protein Transport</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Transcription factors</subject><subject>Translocation</subject><issn>0388-6107</issn><issn>1880-313X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkM1rGzEQxUVpaZy095zCQi89dB1JY-1qj8WkTSDgSwuBHsSsNI7l7IcraSH-76tg15Cchpn5vcfjMXYp-FxKya9bP_bkAsU5NHOpxDs2E1rzEgQ8vGczDlqXleD1GTuPccvzLjR8ZGfAAWABcsb-iNW3QvJV6TxaSvuueMKeWnzCKfih2IUxkU2xwEf0Q0zFC4S9H8bdhobSD26y5IoN7TCNaXz21qd9kYW9t_SJfVhjF-nzcV6w3z9ufi1vy_vVz7vl9_vSqoqn0rnG8TVxm_M1lcuZlaq0qqVrGiGUbAC0061qW127ijIj19JitchXh4Bwwb4efHPavxPFZHofLXUdDjRO0UghpWok1DKjX96g23EKQ05npFwIqEGDyhQ_UDaMMQZam13wPYa9Edy8FG9OxRtoTC4-S66OxlObPyfB_6YzsDwA25jwkU4AhuRtR68d1dH29LUbDIYG-AcYXpkw</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>YOSHIOKA, Hiroki</creator><creator>NONOGAKI, Tsunemasa</creator><creator>OHNISHI, Hiroyuki</creator><creator>FUKUISHI, Nobuyuki</creator><creator>YOSHIKAWA, Masae</creator><creator>GUI, Ming-Yu</creator><creator>JIN, Yong-Ri</creator><creator>LI, Xu-Wen</creator><creator>ADACHI, Yoshiyuki</creator><creator>OHNO, Naohito</creator><creator>TAKEYA, Koichi</creator><creator>HITOTSUYANAGI, Yukio</creator><creator>MIURA, Nobuhiko</creator><creator>AOYAGI, Yutaka</creator><general>Biomedical Research Press</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>7QO</scope><scope>7QP</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20181001</creationdate><title>1O, 20O-diacetyl kamebakaurin protects against acetaminophen-induced hepatotoxicity in mice</title><author>YOSHIOKA, Hiroki ; NONOGAKI, Tsunemasa ; OHNISHI, Hiroyuki ; FUKUISHI, Nobuyuki ; YOSHIKAWA, Masae ; GUI, Ming-Yu ; JIN, Yong-Ri ; LI, Xu-Wen ; ADACHI, Yoshiyuki ; OHNO, Naohito ; TAKEYA, Koichi ; HITOTSUYANAGI, Yukio ; MIURA, Nobuhiko ; AOYAGI, Yutaka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c560t-dd9d0fe0c00396d3885568572d9911529338d8b5bb87d6e3962f2ca648d8da3a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acetaminophen</topic><topic>Acetaminophen - adverse effects</topic><topic>Activation</topic><topic>Analgesics</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Antioxidants - chemistry</topic><topic>Antioxidants - pharmacology</topic><topic>Biomarkers</topic><topic>c-Jun protein</topic><topic>Chemical activity</topic><topic>Chemical and Drug Induced Liver Injury - drug therapy</topic><topic>Chemical and Drug Induced Liver Injury - metabolism</topic><topic>Chemical and Drug Induced Liver Injury - pathology</topic><topic>Chemicals</topic><topic>CYP1A2 protein</topic><topic>Cytochrome P450</topic><topic>Cytokines - metabolism</topic><topic>Deactivation</topic><topic>Diacetyl</topic><topic>Disease Models, Animal</topic><topic>Diterpenes - chemistry</topic><topic>Diterpenes - pharmacology</topic><topic>Ethanol</topic><topic>Gene expression</topic><topic>Glutathione - metabolism</topic><topic>Hepatotoxicity</topic><topic>Inactivation</topic><topic>Inflammation</topic><topic>Inflammation Mediators - metabolism</topic><topic>Inhibition</topic><topic>Injury analysis</topic><topic>JNK protein</topic><topic>Kinases</topic><topic>Liver</topic><topic>Liver Function Tests</topic><topic>Male</topic><topic>Malondialdehyde - metabolism</topic><topic>Mice</topic><topic>Molecular Structure</topic><topic>NF-κB protein</topic><topic>Oils & fats</topic><topic>Olive oil</topic><topic>Oral administration</topic><topic>Organic chemistry</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Protective Agents - chemistry</topic><topic>Protective Agents - pharmacology</topic><topic>Protein Transport</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Transcription factors</topic><topic>Translocation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>YOSHIOKA, Hiroki</creatorcontrib><creatorcontrib>NONOGAKI, Tsunemasa</creatorcontrib><creatorcontrib>OHNISHI, Hiroyuki</creatorcontrib><creatorcontrib>FUKUISHI, Nobuyuki</creatorcontrib><creatorcontrib>YOSHIKAWA, Masae</creatorcontrib><creatorcontrib>GUI, Ming-Yu</creatorcontrib><creatorcontrib>JIN, Yong-Ri</creatorcontrib><creatorcontrib>LI, Xu-Wen</creatorcontrib><creatorcontrib>ADACHI, Yoshiyuki</creatorcontrib><creatorcontrib>OHNO, Naohito</creatorcontrib><creatorcontrib>TAKEYA, Koichi</creatorcontrib><creatorcontrib>HITOTSUYANAGI, Yukio</creatorcontrib><creatorcontrib>MIURA, Nobuhiko</creatorcontrib><creatorcontrib>AOYAGI, Yutaka</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biomedical Research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>YOSHIOKA, Hiroki</au><au>NONOGAKI, Tsunemasa</au><au>OHNISHI, Hiroyuki</au><au>FUKUISHI, Nobuyuki</au><au>YOSHIKAWA, Masae</au><au>GUI, Ming-Yu</au><au>JIN, Yong-Ri</au><au>LI, Xu-Wen</au><au>ADACHI, Yoshiyuki</au><au>OHNO, Naohito</au><au>TAKEYA, Koichi</au><au>HITOTSUYANAGI, Yukio</au><au>MIURA, Nobuhiko</au><au>AOYAGI, Yutaka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>1O, 20O-diacetyl kamebakaurin protects against acetaminophen-induced hepatotoxicity in mice</atitle><jtitle>Biomedical Research</jtitle><addtitle>Biomed. Res.</addtitle><date>2018-10-01</date><risdate>2018</risdate><volume>39</volume><issue>5</issue><spage>251</spage><epage>260</epage><pages>251-260</pages><issn>0388-6107</issn><eissn>1880-313X</eissn><abstract>The present study aimed to investigate the protective effects of kamebakaurin (KA) and 1O, 20O-diacetyl kamebakaurin (Ac2KA) on acetaminophen (APAP)-induced hepatotoxicity and compare the hepatoprotective mechanisms of the two chemicals. Seven-week-old male C57BL/6J mice were orally administered KA, Ac2KA, or an ethanol/olive oil emulsion once per day for 7-days. Twenty-four hours after the final administration, the mice were fasted and then intraperitoneally injected with 450 mg/kg APAP or saline. At 16 h after injection, the mice were euthanized and blood samples were collected for plasma analysis. Pretreatment with KA and Ac2KA significantly attenuated APAP-induced hepatic injury. The protective effect of Ac2KA was stronger than that of KA. These two chemicals attenuated oxidative stress, inflammatory cytokine production, c-jun N-terminal kinase activation, and receptor-interacting protein (RIP)-3 activation. Ac2KA also decreased APAP-induced RIP-1 activation and nuclear factor kappa B (NF-κB) p65 translocation. Moreover, Ac2KA repressed mRNA expression of Cyp1a2/2e1 in the liver. Our results showed that KA and Ac2KA exerted protective effects against APAP-induced hepatotoxicity. The responsible mechanisms may be related to the chemicals’ antioxidant activity and the inhibition of c-jun N-terminal kinase activation and RIP-3 activation. The effects of Ac2KA included those of KA, as well as RIP-1 inactivation, NF-κB inhibition, and Cyp inhibition.</abstract><cop>Japan</cop><pub>Biomedical Research Press</pub><pmid>30333432</pmid><doi>10.2220/biomedres.39.251</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Biomedical Research, 2018/10/01, Vol.39(5), pp.251-260 |
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| subjects | Acetaminophen Acetaminophen - adverse effects Activation Analgesics Animals Antioxidants Antioxidants - chemistry Antioxidants - pharmacology Biomarkers c-Jun protein Chemical activity Chemical and Drug Induced Liver Injury - drug therapy Chemical and Drug Induced Liver Injury - metabolism Chemical and Drug Induced Liver Injury - pathology Chemicals CYP1A2 protein Cytochrome P450 Cytokines - metabolism Deactivation Diacetyl Disease Models, Animal Diterpenes - chemistry Diterpenes - pharmacology Ethanol Gene expression Glutathione - metabolism Hepatotoxicity Inactivation Inflammation Inflammation Mediators - metabolism Inhibition Injury analysis JNK protein Kinases Liver Liver Function Tests Male Malondialdehyde - metabolism Mice Molecular Structure NF-κB protein Oils & fats Olive oil Oral administration Organic chemistry Oxidative stress Oxidative Stress - drug effects Protective Agents - chemistry Protective Agents - pharmacology Protein Transport Reactive Oxygen Species - metabolism Transcription factors Translocation |
| title | 1O, 20O-diacetyl kamebakaurin protects against acetaminophen-induced hepatotoxicity in mice |
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