Acetaminophen attenuates lipopolysaccharide-induced cognitive impairment through antioxidant activity
Considerable evidence has shown that neuroinflammation and oxidative stress play an important role in the pathophysiology of postoperative cognitive dysfunction (POCD) and other progressive neurodegenerative disorders. Increasing evidence suggests that acetaminophen (APAP) has unappreciated antioxid...
Gespeichert in:
| Veröffentlicht in: | Journal of neuroinflammation 2017-01, Vol.14 (1), p.17, Article 17 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 1 |
| container_start_page | 17 |
| container_title | Journal of neuroinflammation |
| container_volume | 14 |
| creator | Zhao, Wei-Xing Zhang, Jun-Han Cao, Jiang-Bei Wang, Wei Wang, Dong-Xin Zhang, Xiao-Ying Yu, Jun Zhang, Yong-Yi Zhang, You-Zhi Mi, Wei-Dong |
| description | Considerable evidence has shown that neuroinflammation and oxidative stress play an important role in the pathophysiology of postoperative cognitive dysfunction (POCD) and other progressive neurodegenerative disorders. Increasing evidence suggests that acetaminophen (APAP) has unappreciated antioxidant and anti-inflammatory properties. However, the impact of APAP on the cognitive sequelae of inflammatory and oxidative stress is unknown. The objective of this study is to explore whether APAP could have neuroprotective effects on lipopolysaccharide (LPS)-induced cognitive impairment in mice.
A mouse model of LPS-induced cognitive impairment was established to evaluate the neuroprotective effects of APAP against LPS-induced cognitive impairment. Adult C57BL/6 mice were treated with APAP half an hour prior to intracerebroventricular microinjection of LPS and every day thereafter, until the end of the study period. The Morris water maze was used to assess cognitive function from postinjection days 1 to 3. Animal behavioural tests as well as pathological and biochemical assays were performed to evaluate LPS-induced hippocampal damage and the neuroprotective effect of APAP.
Mice treated with LPS exhibited impaired performance in the Morris water maze without changing spontaneous locomotor activity, which was ameliorated by treatment with APAP. APAP suppressed the accumulation of pro-inflammatory cytokines and microglial activation induced by LPS in the hippocampus. In addition, APAP increased SOD activity, reduced MDA levels, modulated glycogen synthase kinase 3β (GSK3β) activity and elevated brain-derived neurotrophic factor (BDNF) expression in the hippocampus. Moreover, APAP significantly decreased the Bax/Bcl-2 ratio and neuron apoptosis in the hippocampus of LPS-treated mice.
Our results suggest that APAP may possess a neuroprotective effect against LPS-induced cognitive impairment and inflammatory and oxidative stress via mechanisms involving its antioxidant and anti-inflammatory properties, as well as its ability to inhibit the mitochondrial permeability transition (MPT) pore and the subsequent apoptotic pathway. |
| doi_str_mv | 10.1186/s12974-016-0781-6 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5251335</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A478556695</galeid><sourcerecordid>A478556695</sourcerecordid><originalsourceid>FETCH-LOGICAL-c494t-c31fe9b411c0e4c90e15932f7cbc3527a45e5a7c82914ca2e2e55b43e637d13</originalsourceid><addsrcrecordid>eNptkUtr3DAUhUVpaZ4_oJti6Nqp3rY3hSH0EQhkke6F5vp6rGBLriSHzr-vhknTBIoWV0jnfBzpEPKB0SvGWv05Md41sqZM17RpWa3fkFPWSF5z2sm3L_Yn5CylB0oFV5q_Jye8ZbTjrT4luAHMdnY-LCP6yuaMfrUZUzW5JSxh2icLMNroeqyd71fAvoKw8y67R6zcvFgXZ_S5ymMM626srM8u_HZ9mZWFonJ5f0HeDXZKePk0z8n9t68_r3_Ut3ffb643tzXITuYaBBuw20rGgKKEjiJTneBDA1sQijdWKlS2gZZ3TILlyFGprRSoRdMzcU6-HKnLup2xh5Iq2sks0c027k2wzry-8W40u_BoFFdMCFUAn54AMfxaMWXzENboS2JTvltRLrWW_1Q7O6FxfggFBrNLYDayaZXSujuwrv6jKqvH2UHwOLhy_srAjgaIIaWIw3NwRs2hbnOs25S6zaFuo4vn48sXPzv-9iv-AAuMqFI</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1865024664</pqid></control><display><type>article</type><title>Acetaminophen attenuates lipopolysaccharide-induced cognitive impairment through antioxidant activity</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>SpringerLink Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>PubMed Central Open Access</source><source>Springer Nature OA Free Journals</source><creator>Zhao, Wei-Xing ; Zhang, Jun-Han ; Cao, Jiang-Bei ; Wang, Wei ; Wang, Dong-Xin ; Zhang, Xiao-Ying ; Yu, Jun ; Zhang, Yong-Yi ; Zhang, You-Zhi ; Mi, Wei-Dong</creator><creatorcontrib>Zhao, Wei-Xing ; Zhang, Jun-Han ; Cao, Jiang-Bei ; Wang, Wei ; Wang, Dong-Xin ; Zhang, Xiao-Ying ; Yu, Jun ; Zhang, Yong-Yi ; Zhang, You-Zhi ; Mi, Wei-Dong</creatorcontrib><description>Considerable evidence has shown that neuroinflammation and oxidative stress play an important role in the pathophysiology of postoperative cognitive dysfunction (POCD) and other progressive neurodegenerative disorders. Increasing evidence suggests that acetaminophen (APAP) has unappreciated antioxidant and anti-inflammatory properties. However, the impact of APAP on the cognitive sequelae of inflammatory and oxidative stress is unknown. The objective of this study is to explore whether APAP could have neuroprotective effects on lipopolysaccharide (LPS)-induced cognitive impairment in mice.
A mouse model of LPS-induced cognitive impairment was established to evaluate the neuroprotective effects of APAP against LPS-induced cognitive impairment. Adult C57BL/6 mice were treated with APAP half an hour prior to intracerebroventricular microinjection of LPS and every day thereafter, until the end of the study period. The Morris water maze was used to assess cognitive function from postinjection days 1 to 3. Animal behavioural tests as well as pathological and biochemical assays were performed to evaluate LPS-induced hippocampal damage and the neuroprotective effect of APAP.
Mice treated with LPS exhibited impaired performance in the Morris water maze without changing spontaneous locomotor activity, which was ameliorated by treatment with APAP. APAP suppressed the accumulation of pro-inflammatory cytokines and microglial activation induced by LPS in the hippocampus. In addition, APAP increased SOD activity, reduced MDA levels, modulated glycogen synthase kinase 3β (GSK3β) activity and elevated brain-derived neurotrophic factor (BDNF) expression in the hippocampus. Moreover, APAP significantly decreased the Bax/Bcl-2 ratio and neuron apoptosis in the hippocampus of LPS-treated mice.
Our results suggest that APAP may possess a neuroprotective effect against LPS-induced cognitive impairment and inflammatory and oxidative stress via mechanisms involving its antioxidant and anti-inflammatory properties, as well as its ability to inhibit the mitochondrial permeability transition (MPT) pore and the subsequent apoptotic pathway.</description><identifier>ISSN: 1742-2094</identifier><identifier>EISSN: 1742-2094</identifier><identifier>DOI: 10.1186/s12974-016-0781-6</identifier><identifier>PMID: 28109286</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Acetaminophen ; Acetaminophen - pharmacology ; Animals ; Antioxidants ; Antioxidants - pharmacology ; Cognition disorders ; Cognitive Dysfunction - chemically induced ; Dosage and administration ; Drug therapy ; Hippocampus - drug effects ; Lipopolysaccharides ; Lipopolysaccharides - toxicity ; Male ; Maze Learning - drug effects ; Mice ; Mice, Inbred C57BL ; Motor Activity - drug effects ; Neuroprotective Agents - pharmacology</subject><ispartof>Journal of neuroinflammation, 2017-01, Vol.14 (1), p.17, Article 17</ispartof><rights>COPYRIGHT 2017 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2017</rights><rights>The Author(s). 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-c31fe9b411c0e4c90e15932f7cbc3527a45e5a7c82914ca2e2e55b43e637d13</citedby><cites>FETCH-LOGICAL-c494t-c31fe9b411c0e4c90e15932f7cbc3527a45e5a7c82914ca2e2e55b43e637d13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5251335/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5251335/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28109286$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Wei-Xing</creatorcontrib><creatorcontrib>Zhang, Jun-Han</creatorcontrib><creatorcontrib>Cao, Jiang-Bei</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Wang, Dong-Xin</creatorcontrib><creatorcontrib>Zhang, Xiao-Ying</creatorcontrib><creatorcontrib>Yu, Jun</creatorcontrib><creatorcontrib>Zhang, Yong-Yi</creatorcontrib><creatorcontrib>Zhang, You-Zhi</creatorcontrib><creatorcontrib>Mi, Wei-Dong</creatorcontrib><title>Acetaminophen attenuates lipopolysaccharide-induced cognitive impairment through antioxidant activity</title><title>Journal of neuroinflammation</title><addtitle>J Neuroinflammation</addtitle><description>Considerable evidence has shown that neuroinflammation and oxidative stress play an important role in the pathophysiology of postoperative cognitive dysfunction (POCD) and other progressive neurodegenerative disorders. Increasing evidence suggests that acetaminophen (APAP) has unappreciated antioxidant and anti-inflammatory properties. However, the impact of APAP on the cognitive sequelae of inflammatory and oxidative stress is unknown. The objective of this study is to explore whether APAP could have neuroprotective effects on lipopolysaccharide (LPS)-induced cognitive impairment in mice.
A mouse model of LPS-induced cognitive impairment was established to evaluate the neuroprotective effects of APAP against LPS-induced cognitive impairment. Adult C57BL/6 mice were treated with APAP half an hour prior to intracerebroventricular microinjection of LPS and every day thereafter, until the end of the study period. The Morris water maze was used to assess cognitive function from postinjection days 1 to 3. Animal behavioural tests as well as pathological and biochemical assays were performed to evaluate LPS-induced hippocampal damage and the neuroprotective effect of APAP.
Mice treated with LPS exhibited impaired performance in the Morris water maze without changing spontaneous locomotor activity, which was ameliorated by treatment with APAP. APAP suppressed the accumulation of pro-inflammatory cytokines and microglial activation induced by LPS in the hippocampus. In addition, APAP increased SOD activity, reduced MDA levels, modulated glycogen synthase kinase 3β (GSK3β) activity and elevated brain-derived neurotrophic factor (BDNF) expression in the hippocampus. Moreover, APAP significantly decreased the Bax/Bcl-2 ratio and neuron apoptosis in the hippocampus of LPS-treated mice.
Our results suggest that APAP may possess a neuroprotective effect against LPS-induced cognitive impairment and inflammatory and oxidative stress via mechanisms involving its antioxidant and anti-inflammatory properties, as well as its ability to inhibit the mitochondrial permeability transition (MPT) pore and the subsequent apoptotic pathway.</description><subject>Acetaminophen</subject><subject>Acetaminophen - pharmacology</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Cognition disorders</subject><subject>Cognitive Dysfunction - chemically induced</subject><subject>Dosage and administration</subject><subject>Drug therapy</subject><subject>Hippocampus - drug effects</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - toxicity</subject><subject>Male</subject><subject>Maze Learning - drug effects</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Motor Activity - drug effects</subject><subject>Neuroprotective Agents - pharmacology</subject><issn>1742-2094</issn><issn>1742-2094</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkUtr3DAUhUVpaZ4_oJti6Nqp3rY3hSH0EQhkke6F5vp6rGBLriSHzr-vhknTBIoWV0jnfBzpEPKB0SvGWv05Md41sqZM17RpWa3fkFPWSF5z2sm3L_Yn5CylB0oFV5q_Jye8ZbTjrT4luAHMdnY-LCP6yuaMfrUZUzW5JSxh2icLMNroeqyd71fAvoKw8y67R6zcvFgXZ_S5ymMM626srM8u_HZ9mZWFonJ5f0HeDXZKePk0z8n9t68_r3_Ut3ffb643tzXITuYaBBuw20rGgKKEjiJTneBDA1sQijdWKlS2gZZ3TILlyFGprRSoRdMzcU6-HKnLup2xh5Iq2sks0c027k2wzry-8W40u_BoFFdMCFUAn54AMfxaMWXzENboS2JTvltRLrWW_1Q7O6FxfggFBrNLYDayaZXSujuwrv6jKqvH2UHwOLhy_srAjgaIIaWIw3NwRs2hbnOs25S6zaFuo4vn48sXPzv-9iv-AAuMqFI</recordid><startdate>20170121</startdate><enddate>20170121</enddate><creator>Zhao, Wei-Xing</creator><creator>Zhang, Jun-Han</creator><creator>Cao, Jiang-Bei</creator><creator>Wang, Wei</creator><creator>Wang, Dong-Xin</creator><creator>Zhang, Xiao-Ying</creator><creator>Yu, Jun</creator><creator>Zhang, Yong-Yi</creator><creator>Zhang, You-Zhi</creator><creator>Mi, Wei-Dong</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>3V.</scope><scope>7T5</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20170121</creationdate><title>Acetaminophen attenuates lipopolysaccharide-induced cognitive impairment through antioxidant activity</title><author>Zhao, Wei-Xing ; Zhang, Jun-Han ; Cao, Jiang-Bei ; Wang, Wei ; Wang, Dong-Xin ; Zhang, Xiao-Ying ; Yu, Jun ; Zhang, Yong-Yi ; Zhang, You-Zhi ; Mi, Wei-Dong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-c31fe9b411c0e4c90e15932f7cbc3527a45e5a7c82914ca2e2e55b43e637d13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Acetaminophen</topic><topic>Acetaminophen - pharmacology</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Cognition disorders</topic><topic>Cognitive Dysfunction - chemically induced</topic><topic>Dosage and administration</topic><topic>Drug therapy</topic><topic>Hippocampus - drug effects</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - toxicity</topic><topic>Male</topic><topic>Maze Learning - drug effects</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Motor Activity - drug effects</topic><topic>Neuroprotective Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Wei-Xing</creatorcontrib><creatorcontrib>Zhang, Jun-Han</creatorcontrib><creatorcontrib>Cao, Jiang-Bei</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Wang, Dong-Xin</creatorcontrib><creatorcontrib>Zhang, Xiao-Ying</creatorcontrib><creatorcontrib>Yu, Jun</creatorcontrib><creatorcontrib>Zhang, Yong-Yi</creatorcontrib><creatorcontrib>Zhang, You-Zhi</creatorcontrib><creatorcontrib>Mi, Wei-Dong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neuroinflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Wei-Xing</au><au>Zhang, Jun-Han</au><au>Cao, Jiang-Bei</au><au>Wang, Wei</au><au>Wang, Dong-Xin</au><au>Zhang, Xiao-Ying</au><au>Yu, Jun</au><au>Zhang, Yong-Yi</au><au>Zhang, You-Zhi</au><au>Mi, Wei-Dong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acetaminophen attenuates lipopolysaccharide-induced cognitive impairment through antioxidant activity</atitle><jtitle>Journal of neuroinflammation</jtitle><addtitle>J Neuroinflammation</addtitle><date>2017-01-21</date><risdate>2017</risdate><volume>14</volume><issue>1</issue><spage>17</spage><pages>17-</pages><artnum>17</artnum><issn>1742-2094</issn><eissn>1742-2094</eissn><abstract>Considerable evidence has shown that neuroinflammation and oxidative stress play an important role in the pathophysiology of postoperative cognitive dysfunction (POCD) and other progressive neurodegenerative disorders. Increasing evidence suggests that acetaminophen (APAP) has unappreciated antioxidant and anti-inflammatory properties. However, the impact of APAP on the cognitive sequelae of inflammatory and oxidative stress is unknown. The objective of this study is to explore whether APAP could have neuroprotective effects on lipopolysaccharide (LPS)-induced cognitive impairment in mice.
A mouse model of LPS-induced cognitive impairment was established to evaluate the neuroprotective effects of APAP against LPS-induced cognitive impairment. Adult C57BL/6 mice were treated with APAP half an hour prior to intracerebroventricular microinjection of LPS and every day thereafter, until the end of the study period. The Morris water maze was used to assess cognitive function from postinjection days 1 to 3. Animal behavioural tests as well as pathological and biochemical assays were performed to evaluate LPS-induced hippocampal damage and the neuroprotective effect of APAP.
Mice treated with LPS exhibited impaired performance in the Morris water maze without changing spontaneous locomotor activity, which was ameliorated by treatment with APAP. APAP suppressed the accumulation of pro-inflammatory cytokines and microglial activation induced by LPS in the hippocampus. In addition, APAP increased SOD activity, reduced MDA levels, modulated glycogen synthase kinase 3β (GSK3β) activity and elevated brain-derived neurotrophic factor (BDNF) expression in the hippocampus. Moreover, APAP significantly decreased the Bax/Bcl-2 ratio and neuron apoptosis in the hippocampus of LPS-treated mice.
Our results suggest that APAP may possess a neuroprotective effect against LPS-induced cognitive impairment and inflammatory and oxidative stress via mechanisms involving its antioxidant and anti-inflammatory properties, as well as its ability to inhibit the mitochondrial permeability transition (MPT) pore and the subsequent apoptotic pathway.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>28109286</pmid><doi>10.1186/s12974-016-0781-6</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1742-2094 |
| ispartof | Journal of neuroinflammation, 2017-01, Vol.14 (1), p.17, Article 17 |
| issn | 1742-2094 1742-2094 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5251335 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; SpringerLink Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access; Springer Nature OA Free Journals |
| subjects | Acetaminophen Acetaminophen - pharmacology Animals Antioxidants Antioxidants - pharmacology Cognition disorders Cognitive Dysfunction - chemically induced Dosage and administration Drug therapy Hippocampus - drug effects Lipopolysaccharides Lipopolysaccharides - toxicity Male Maze Learning - drug effects Mice Mice, Inbred C57BL Motor Activity - drug effects Neuroprotective Agents - pharmacology |
| title | Acetaminophen attenuates lipopolysaccharide-induced cognitive impairment through antioxidant activity |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-09T07%3A23%3A04IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Acetaminophen%20attenuates%20lipopolysaccharide-induced%20cognitive%20impairment%20through%20antioxidant%20activity&rft.jtitle=Journal%20of%20neuroinflammation&rft.au=Zhao,%20Wei-Xing&rft.date=2017-01-21&rft.volume=14&rft.issue=1&rft.spage=17&rft.pages=17-&rft.artnum=17&rft.issn=1742-2094&rft.eissn=1742-2094&rft_id=info:doi/10.1186/s12974-016-0781-6&rft_dat=%3Cgale_pubme%3EA478556695%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1865024664&rft_id=info:pmid/28109286&rft_galeid=A478556695&rfr_iscdi=true |