The Proton Pump Inhibitor Lansoprazole Has Hepatoprotective Effects in In Vitro and In Vivo Rat Models of Acute Liver Injury
Background/Aims The proton pump inhibitor lansoprazole (LPZ) is clinically used to reduce gastric acid secretion, but little is known about its possible hepatoprotective effects. This study aimed to investigate the hepatoprotective effects of LPZ and its potential mechanisms using in vitro and in vi...
Gespeichert in:
| Veröffentlicht in: | Digestive diseases and sciences 2019-10, Vol.64 (10), p.2854-2866 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2866 |
|---|---|
| container_issue | 10 |
| container_start_page | 2854 |
| container_title | Digestive diseases and sciences |
| container_volume | 64 |
| creator | Nakatake, Richi Hishikawa, Hidehiko Kotsuka, Masaya Ishizaki, Morihiko Matsui, Kosuke Nishizawa, Mikio Yoshizawa, Katsuhiko Kaibori, Masaki Okumura, Tadayoshi |
| description | Background/Aims
The proton pump inhibitor lansoprazole (LPZ) is clinically used to reduce gastric acid secretion, but little is known about its possible hepatoprotective effects. This study aimed to investigate the hepatoprotective effects of LPZ and its potential mechanisms using in vitro and in vivo rat models of liver injury.
Methods
For the in vitro model of liver injury, primary cultured rat hepatocytes were treated with interleukin-1β in the presence or absence of LPZ. The influence of LPZ on inducible nitric oxide synthase (iNOS) induction and nitric oxide (NO) production and on the associated signaling pathways was analyzed. For the in vivo model, rats were treated with D-galactosamine (GalN) and lipopolysaccharide (LPS). The effects of LPZ on survival and proinflammatory mediator expression (including iNOS and tumor necrosis factor-α) in these rats were examined.
Results
LPZ inhibited iNOS induction partially through suppression of the nuclear factor-kappa B signaling pathway in hepatocytes, thereby reducing potential liver injury from excessive NO levels. Additionally, LPZ increased survival by 50% and decreased iNOS, tumor necrosis factor-α, and cytokine-induced neutrophil chemoattractant-1 mRNA expression in the livers of GalN/LPS-treated rats. LPZ also inhibited nuclear factor-kappa B activation by GalN/LPS.
Conclusions
LPZ inhibits the induction of several inflammatory mediators (including cytokines, chemokines, and NO) partially through suppression of nuclear factor-kappa B, resulting in the prevention of fulminant liver failure. The therapeutic potential of LPZ for liver injuries warrants further investigation. |
| doi_str_mv | 10.1007/s10620-019-05622-6 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_2210258963</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A712936666</galeid><sourcerecordid>A712936666</sourcerecordid><originalsourceid>FETCH-LOGICAL-c508t-5e7252ed46ec44a387f8f50936fc6633f0c31b88454dac686f7fafd566255b9e3</originalsourceid><addsrcrecordid>eNp9kV9vFCEUxYnR2HX1C_hgSHzxZVr-DMzM46apbpM1bZrqK2GZS8tmBlZgmtT44WWdaqMxhQcu8Ds3Bw5Cbyk5poQ0J4kSyUhFaFcRIRmr5DO0oKLhFROyfY4WhMpSUyqP0KuUdoSQrqHyJTripGu7WvIF-nF9C_gyhhw8vpzGPT73t27rcoh4o30K-6i_hwHwWie8hr3O5SRkMNndAT6ztlQJO19k-KvLMWDt-3lzF_CVzvhz6GFIOFi8MlMGvCnCWIjdFO9foxdWDwnePKxL9OXj2fXputpcfDo_XW0qI0ibKwENEwz6WoKpa83bxrZWkI5La6Tk3BLD6bZta1H32shW2sZq2wspmRDbDvgSfZj7Fu_fJkhZjS4ZGAbtIUxJMUYJE21Xei3R-3_QXZiiL-4KVb6vo5TVj9SNHkA5b0OO2hyaqlVDWXFWRqGO_0OV2cPoTPBgXTn_S8BmgYkhpQhW7aMbdbxXlKhD5GqOXJXI1a_I1UH07sHxtB2h_yP5nXEB-AykcuVvID4-6Ym2PwFWc7Rc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2209791124</pqid></control><display><type>article</type><title>The Proton Pump Inhibitor Lansoprazole Has Hepatoprotective Effects in In Vitro and In Vivo Rat Models of Acute Liver Injury</title><source>MEDLINE</source><source>SpringerLink (Online service)</source><creator>Nakatake, Richi ; Hishikawa, Hidehiko ; Kotsuka, Masaya ; Ishizaki, Morihiko ; Matsui, Kosuke ; Nishizawa, Mikio ; Yoshizawa, Katsuhiko ; Kaibori, Masaki ; Okumura, Tadayoshi</creator><creatorcontrib>Nakatake, Richi ; Hishikawa, Hidehiko ; Kotsuka, Masaya ; Ishizaki, Morihiko ; Matsui, Kosuke ; Nishizawa, Mikio ; Yoshizawa, Katsuhiko ; Kaibori, Masaki ; Okumura, Tadayoshi</creatorcontrib><description>Background/Aims
The proton pump inhibitor lansoprazole (LPZ) is clinically used to reduce gastric acid secretion, but little is known about its possible hepatoprotective effects. This study aimed to investigate the hepatoprotective effects of LPZ and its potential mechanisms using in vitro and in vivo rat models of liver injury.
Methods
For the in vitro model of liver injury, primary cultured rat hepatocytes were treated with interleukin-1β in the presence or absence of LPZ. The influence of LPZ on inducible nitric oxide synthase (iNOS) induction and nitric oxide (NO) production and on the associated signaling pathways was analyzed. For the in vivo model, rats were treated with D-galactosamine (GalN) and lipopolysaccharide (LPS). The effects of LPZ on survival and proinflammatory mediator expression (including iNOS and tumor necrosis factor-α) in these rats were examined.
Results
LPZ inhibited iNOS induction partially through suppression of the nuclear factor-kappa B signaling pathway in hepatocytes, thereby reducing potential liver injury from excessive NO levels. Additionally, LPZ increased survival by 50% and decreased iNOS, tumor necrosis factor-α, and cytokine-induced neutrophil chemoattractant-1 mRNA expression in the livers of GalN/LPS-treated rats. LPZ also inhibited nuclear factor-kappa B activation by GalN/LPS.
Conclusions
LPZ inhibits the induction of several inflammatory mediators (including cytokines, chemokines, and NO) partially through suppression of nuclear factor-kappa B, resulting in the prevention of fulminant liver failure. The therapeutic potential of LPZ for liver injuries warrants further investigation.</description><identifier>ISSN: 0163-2116</identifier><identifier>EISSN: 1573-2568</identifier><identifier>DOI: 10.1007/s10620-019-05622-6</identifier><identifier>PMID: 30989463</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Aprotinin ; Biochemistry ; Cells, Cultured ; Disease Models, Animal ; Gastroenterology ; Hepatocytes - drug effects ; Hepatocytes - metabolism ; Hepatology ; Inhibitor drugs ; Interleukins ; Lansoprazole ; Lansoprazole - pharmacology ; Liver ; Liver - drug effects ; Liver diseases ; Liver Failure, Acute - chemically induced ; Liver Failure, Acute - metabolism ; Liver Failure, Acute - prevention & control ; Mediation ; Medicine ; Medicine & Public Health ; NF-kappa B - metabolism ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type II - metabolism ; Oncology ; Original Article ; Protective Agents - pharmacology ; Proton Pump Inhibitors - pharmacology ; Rats ; Rodents ; Transplant Surgery ; Treatment Outcome ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF</subject><ispartof>Digestive diseases and sciences, 2019-10, Vol.64 (10), p.2854-2866</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>COPYRIGHT 2019 Springer</rights><rights>Digestive Diseases and Sciences is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-5e7252ed46ec44a387f8f50936fc6633f0c31b88454dac686f7fafd566255b9e3</citedby><cites>FETCH-LOGICAL-c508t-5e7252ed46ec44a387f8f50936fc6633f0c31b88454dac686f7fafd566255b9e3</cites><orcidid>0000-0002-7909-9570</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10620-019-05622-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10620-019-05622-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30989463$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nakatake, Richi</creatorcontrib><creatorcontrib>Hishikawa, Hidehiko</creatorcontrib><creatorcontrib>Kotsuka, Masaya</creatorcontrib><creatorcontrib>Ishizaki, Morihiko</creatorcontrib><creatorcontrib>Matsui, Kosuke</creatorcontrib><creatorcontrib>Nishizawa, Mikio</creatorcontrib><creatorcontrib>Yoshizawa, Katsuhiko</creatorcontrib><creatorcontrib>Kaibori, Masaki</creatorcontrib><creatorcontrib>Okumura, Tadayoshi</creatorcontrib><title>The Proton Pump Inhibitor Lansoprazole Has Hepatoprotective Effects in In Vitro and In Vivo Rat Models of Acute Liver Injury</title><title>Digestive diseases and sciences</title><addtitle>Dig Dis Sci</addtitle><addtitle>Dig Dis Sci</addtitle><description>Background/Aims
The proton pump inhibitor lansoprazole (LPZ) is clinically used to reduce gastric acid secretion, but little is known about its possible hepatoprotective effects. This study aimed to investigate the hepatoprotective effects of LPZ and its potential mechanisms using in vitro and in vivo rat models of liver injury.
Methods
For the in vitro model of liver injury, primary cultured rat hepatocytes were treated with interleukin-1β in the presence or absence of LPZ. The influence of LPZ on inducible nitric oxide synthase (iNOS) induction and nitric oxide (NO) production and on the associated signaling pathways was analyzed. For the in vivo model, rats were treated with D-galactosamine (GalN) and lipopolysaccharide (LPS). The effects of LPZ on survival and proinflammatory mediator expression (including iNOS and tumor necrosis factor-α) in these rats were examined.
Results
LPZ inhibited iNOS induction partially through suppression of the nuclear factor-kappa B signaling pathway in hepatocytes, thereby reducing potential liver injury from excessive NO levels. Additionally, LPZ increased survival by 50% and decreased iNOS, tumor necrosis factor-α, and cytokine-induced neutrophil chemoattractant-1 mRNA expression in the livers of GalN/LPS-treated rats. LPZ also inhibited nuclear factor-kappa B activation by GalN/LPS.
Conclusions
LPZ inhibits the induction of several inflammatory mediators (including cytokines, chemokines, and NO) partially through suppression of nuclear factor-kappa B, resulting in the prevention of fulminant liver failure. The therapeutic potential of LPZ for liver injuries warrants further investigation.</description><subject>Animals</subject><subject>Aprotinin</subject><subject>Biochemistry</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>Gastroenterology</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - metabolism</subject><subject>Hepatology</subject><subject>Inhibitor drugs</subject><subject>Interleukins</subject><subject>Lansoprazole</subject><subject>Lansoprazole - pharmacology</subject><subject>Liver</subject><subject>Liver - drug effects</subject><subject>Liver diseases</subject><subject>Liver Failure, Acute - chemically induced</subject><subject>Liver Failure, Acute - metabolism</subject><subject>Liver Failure, Acute - prevention & control</subject><subject>Mediation</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>NF-kappa B - metabolism</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Protective Agents - pharmacology</subject><subject>Proton Pump Inhibitors - pharmacology</subject><subject>Rats</subject><subject>Rodents</subject><subject>Transplant Surgery</subject><subject>Treatment Outcome</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><issn>0163-2116</issn><issn>1573-2568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kV9vFCEUxYnR2HX1C_hgSHzxZVr-DMzM46apbpM1bZrqK2GZS8tmBlZgmtT44WWdaqMxhQcu8Ds3Bw5Cbyk5poQ0J4kSyUhFaFcRIRmr5DO0oKLhFROyfY4WhMpSUyqP0KuUdoSQrqHyJTripGu7WvIF-nF9C_gyhhw8vpzGPT73t27rcoh4o30K-6i_hwHwWie8hr3O5SRkMNndAT6ztlQJO19k-KvLMWDt-3lzF_CVzvhz6GFIOFi8MlMGvCnCWIjdFO9foxdWDwnePKxL9OXj2fXputpcfDo_XW0qI0ibKwENEwz6WoKpa83bxrZWkI5La6Tk3BLD6bZta1H32shW2sZq2wspmRDbDvgSfZj7Fu_fJkhZjS4ZGAbtIUxJMUYJE21Xei3R-3_QXZiiL-4KVb6vo5TVj9SNHkA5b0OO2hyaqlVDWXFWRqGO_0OV2cPoTPBgXTn_S8BmgYkhpQhW7aMbdbxXlKhD5GqOXJXI1a_I1UH07sHxtB2h_yP5nXEB-AykcuVvID4-6Ym2PwFWc7Rc</recordid><startdate>20191001</startdate><enddate>20191001</enddate><creator>Nakatake, Richi</creator><creator>Hishikawa, Hidehiko</creator><creator>Kotsuka, Masaya</creator><creator>Ishizaki, Morihiko</creator><creator>Matsui, Kosuke</creator><creator>Nishizawa, Mikio</creator><creator>Yoshizawa, Katsuhiko</creator><creator>Kaibori, Masaki</creator><creator>Okumura, Tadayoshi</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</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>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</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>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7909-9570</orcidid></search><sort><creationdate>20191001</creationdate><title>The Proton Pump Inhibitor Lansoprazole Has Hepatoprotective Effects in In Vitro and In Vivo Rat Models of Acute Liver Injury</title><author>Nakatake, Richi ; Hishikawa, Hidehiko ; Kotsuka, Masaya ; Ishizaki, Morihiko ; Matsui, Kosuke ; Nishizawa, Mikio ; Yoshizawa, Katsuhiko ; Kaibori, Masaki ; Okumura, Tadayoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c508t-5e7252ed46ec44a387f8f50936fc6633f0c31b88454dac686f7fafd566255b9e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Aprotinin</topic><topic>Biochemistry</topic><topic>Cells, Cultured</topic><topic>Disease Models, Animal</topic><topic>Gastroenterology</topic><topic>Hepatocytes - drug effects</topic><topic>Hepatocytes - metabolism</topic><topic>Hepatology</topic><topic>Inhibitor drugs</topic><topic>Interleukins</topic><topic>Lansoprazole</topic><topic>Lansoprazole - pharmacology</topic><topic>Liver</topic><topic>Liver - drug effects</topic><topic>Liver diseases</topic><topic>Liver Failure, Acute - chemically induced</topic><topic>Liver Failure, Acute - metabolism</topic><topic>Liver Failure, Acute - prevention & control</topic><topic>Mediation</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>NF-kappa B - metabolism</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Protective Agents - pharmacology</topic><topic>Proton Pump Inhibitors - pharmacology</topic><topic>Rats</topic><topic>Rodents</topic><topic>Transplant Surgery</topic><topic>Treatment Outcome</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nakatake, Richi</creatorcontrib><creatorcontrib>Hishikawa, Hidehiko</creatorcontrib><creatorcontrib>Kotsuka, Masaya</creatorcontrib><creatorcontrib>Ishizaki, Morihiko</creatorcontrib><creatorcontrib>Matsui, Kosuke</creatorcontrib><creatorcontrib>Nishizawa, Mikio</creatorcontrib><creatorcontrib>Yoshizawa, Katsuhiko</creatorcontrib><creatorcontrib>Kaibori, Masaki</creatorcontrib><creatorcontrib>Okumura, Tadayoshi</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>ProQuest Nursing and Allied Health Journals</collection><collection>Health & Medicine (ProQuest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>Consumer Health Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>MEDLINE - Academic</collection><jtitle>Digestive diseases and sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nakatake, Richi</au><au>Hishikawa, Hidehiko</au><au>Kotsuka, Masaya</au><au>Ishizaki, Morihiko</au><au>Matsui, Kosuke</au><au>Nishizawa, Mikio</au><au>Yoshizawa, Katsuhiko</au><au>Kaibori, Masaki</au><au>Okumura, Tadayoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Proton Pump Inhibitor Lansoprazole Has Hepatoprotective Effects in In Vitro and In Vivo Rat Models of Acute Liver Injury</atitle><jtitle>Digestive diseases and sciences</jtitle><stitle>Dig Dis Sci</stitle><addtitle>Dig Dis Sci</addtitle><date>2019-10-01</date><risdate>2019</risdate><volume>64</volume><issue>10</issue><spage>2854</spage><epage>2866</epage><pages>2854-2866</pages><issn>0163-2116</issn><eissn>1573-2568</eissn><abstract>Background/Aims
The proton pump inhibitor lansoprazole (LPZ) is clinically used to reduce gastric acid secretion, but little is known about its possible hepatoprotective effects. This study aimed to investigate the hepatoprotective effects of LPZ and its potential mechanisms using in vitro and in vivo rat models of liver injury.
Methods
For the in vitro model of liver injury, primary cultured rat hepatocytes were treated with interleukin-1β in the presence or absence of LPZ. The influence of LPZ on inducible nitric oxide synthase (iNOS) induction and nitric oxide (NO) production and on the associated signaling pathways was analyzed. For the in vivo model, rats were treated with D-galactosamine (GalN) and lipopolysaccharide (LPS). The effects of LPZ on survival and proinflammatory mediator expression (including iNOS and tumor necrosis factor-α) in these rats were examined.
Results
LPZ inhibited iNOS induction partially through suppression of the nuclear factor-kappa B signaling pathway in hepatocytes, thereby reducing potential liver injury from excessive NO levels. Additionally, LPZ increased survival by 50% and decreased iNOS, tumor necrosis factor-α, and cytokine-induced neutrophil chemoattractant-1 mRNA expression in the livers of GalN/LPS-treated rats. LPZ also inhibited nuclear factor-kappa B activation by GalN/LPS.
Conclusions
LPZ inhibits the induction of several inflammatory mediators (including cytokines, chemokines, and NO) partially through suppression of nuclear factor-kappa B, resulting in the prevention of fulminant liver failure. The therapeutic potential of LPZ for liver injuries warrants further investigation.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>30989463</pmid><doi>10.1007/s10620-019-05622-6</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-7909-9570</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0163-2116 |
| ispartof | Digestive diseases and sciences, 2019-10, Vol.64 (10), p.2854-2866 |
| issn | 0163-2116 1573-2568 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2210258963 |
| source | MEDLINE; SpringerLink (Online service) |
| subjects | Animals Aprotinin Biochemistry Cells, Cultured Disease Models, Animal Gastroenterology Hepatocytes - drug effects Hepatocytes - metabolism Hepatology Inhibitor drugs Interleukins Lansoprazole Lansoprazole - pharmacology Liver Liver - drug effects Liver diseases Liver Failure, Acute - chemically induced Liver Failure, Acute - metabolism Liver Failure, Acute - prevention & control Mediation Medicine Medicine & Public Health NF-kappa B - metabolism Nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase Type II - metabolism Oncology Original Article Protective Agents - pharmacology Proton Pump Inhibitors - pharmacology Rats Rodents Transplant Surgery Treatment Outcome Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF |
| title | The Proton Pump Inhibitor Lansoprazole Has Hepatoprotective Effects in In Vitro and In Vivo Rat Models of Acute Liver Injury |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-17T17%3A34%3A46IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20Proton%20Pump%20Inhibitor%20Lansoprazole%20Has%20Hepatoprotective%20Effects%20in%20In%20Vitro%20and%20In%20Vivo%20Rat%20Models%20of%20Acute%20Liver%20Injury&rft.jtitle=Digestive%20diseases%20and%20sciences&rft.au=Nakatake,%20Richi&rft.date=2019-10-01&rft.volume=64&rft.issue=10&rft.spage=2854&rft.epage=2866&rft.pages=2854-2866&rft.issn=0163-2116&rft.eissn=1573-2568&rft_id=info:doi/10.1007/s10620-019-05622-6&rft_dat=%3Cgale_proqu%3EA712936666%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2209791124&rft_id=info:pmid/30989463&rft_galeid=A712936666&rfr_iscdi=true |