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Apocynin, an NADPH Oxidase Enzyme Inhibitor, Prevents Amebic Liver Abscess in Hamster
Amebiasis is an intestinal infection caused by Entamoeba histolytica. Amebic liver abscess (ALA) is the most common extraintestinal complication of amebiasis. In animal models of ALA, neutrophils have been shown to be the first cells to come into contact with Entamoeba histolytica during the initial...
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Published in: | Biomedicines 2023-08, Vol.11 (8), p.2322 |
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description | Amebiasis is an intestinal infection caused by Entamoeba histolytica. Amebic liver abscess (ALA) is the most common extraintestinal complication of amebiasis. In animal models of ALA, neutrophils have been shown to be the first cells to come into contact with Entamoeba histolytica during the initial phase of ALA. One of the multiple mechanisms by which neutrophils exhibit amebicidal activity is through reactive oxygen species (ROS) and the enzyme NADPH oxidase (NOX2), which generates and transports electrons to subsequently reduce molecular oxygen into superoxide anion. Previous reports have shown that ROS release in the susceptible animal species (hamster) is mainly stimulated by the pathogen, in turn provoking such an exacerbated inflammatory reaction that it is unable to be controlled and results in the death of the animal model. Apocynin is a natural inhibitor of NADPH oxidase. No information is available on the role of NOX in the evolution of ALA in the hamster, a susceptible model. Our study showed that administration of a selective NADPH oxidase 2 (NOX2) enzyme inhibitor significantly decreases the percentage of ALA, the size of inflammatory foci, the number of neutrophils, and NOX activity indicated by the reduction in superoxide anion (O2−) production. Moreover, in vitro, the apocynin damages amoebae. Our results showed that apocynin administration induces a decrease in the activity of NOX that could favor a decrease in ALA progression. |
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Amebic liver abscess (ALA) is the most common extraintestinal complication of amebiasis. In animal models of ALA, neutrophils have been shown to be the first cells to come into contact with Entamoeba histolytica during the initial phase of ALA. One of the multiple mechanisms by which neutrophils exhibit amebicidal activity is through reactive oxygen species (ROS) and the enzyme NADPH oxidase (NOX2), which generates and transports electrons to subsequently reduce molecular oxygen into superoxide anion. Previous reports have shown that ROS release in the susceptible animal species (hamster) is mainly stimulated by the pathogen, in turn provoking such an exacerbated inflammatory reaction that it is unable to be controlled and results in the death of the animal model. Apocynin is a natural inhibitor of NADPH oxidase. No information is available on the role of NOX in the evolution of ALA in the hamster, a susceptible model. Our study showed that administration of a selective NADPH oxidase 2 (NOX2) enzyme inhibitor significantly decreases the percentage of ALA, the size of inflammatory foci, the number of neutrophils, and NOX activity indicated by the reduction in superoxide anion (O2−) production. Moreover, in vitro, the apocynin damages amoebae. Our results showed that apocynin administration induces a decrease in the activity of NOX that could favor a decrease in ALA progression.</description><identifier>ISSN: 2227-9059</identifier><identifier>EISSN: 2227-9059</identifier><identifier>DOI: 10.3390/biomedicines11082322</identifier><identifier>PMID: 37626818</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Abscesses ; Amebiasis ; amebic liver abscess ; Animal models ; apocynin ; CYBB protein ; Drug dosages ; Entamoeba histolytica ; Enzyme inhibitors ; Enzymes ; Gastrointestinal system ; Hamsters ; Health care ; Infections ; Inflammation ; Laboratory animals ; Leukocytes (neutrophilic) ; Liver ; Liver diseases ; Microscopy ; NAD(P)H oxidase ; NADPH oxidase ; neutrophil ; Neutrophils ; NOX2 ; Parasites ; Parasitic diseases ; Photographic industry ; Protozoa ; Reactive oxygen species ; Superoxide anions ; Tropical diseases</subject><ispartof>Biomedicines, 2023-08, Vol.11 (8), p.2322</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 by the authors. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c547t-3a5ce639fdc80305b5083186bfce69add3485230b71c8273fd84860f9a445763</citedby><cites>FETCH-LOGICAL-c547t-3a5ce639fdc80305b5083186bfce69add3485230b71c8273fd84860f9a445763</cites><orcidid>0000-0003-0467-2528 ; 0000-0003-1415-5524 ; 0000-0001-8648-7734 ; 0000-0001-5250-7952 ; 0000-0002-0807-7104 ; 0000-0003-0283-1812</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2856838797/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2856838797?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids></links><search><creatorcontrib>Higuera-Martínez, Germán</creatorcontrib><creatorcontrib>Arciniega-Martínez, Ivonne Maciel</creatorcontrib><creatorcontrib>Jarillo-Luna, Rosa Adriana</creatorcontrib><creatorcontrib>Cárdenas-Jaramillo, Luz María</creatorcontrib><creatorcontrib>Levaro-Loquio, David</creatorcontrib><creatorcontrib>Velásquez-Torres, Maritza</creatorcontrib><creatorcontrib>Abarca-Rojano, Edgar</creatorcontrib><creatorcontrib>Reséndiz-Albor, Aldo Arturo</creatorcontrib><creatorcontrib>Pacheco-Yépez, Judith</creatorcontrib><title>Apocynin, an NADPH Oxidase Enzyme Inhibitor, Prevents Amebic Liver Abscess in Hamster</title><title>Biomedicines</title><description>Amebiasis is an intestinal infection caused by Entamoeba histolytica. Amebic liver abscess (ALA) is the most common extraintestinal complication of amebiasis. In animal models of ALA, neutrophils have been shown to be the first cells to come into contact with Entamoeba histolytica during the initial phase of ALA. One of the multiple mechanisms by which neutrophils exhibit amebicidal activity is through reactive oxygen species (ROS) and the enzyme NADPH oxidase (NOX2), which generates and transports electrons to subsequently reduce molecular oxygen into superoxide anion. Previous reports have shown that ROS release in the susceptible animal species (hamster) is mainly stimulated by the pathogen, in turn provoking such an exacerbated inflammatory reaction that it is unable to be controlled and results in the death of the animal model. Apocynin is a natural inhibitor of NADPH oxidase. No information is available on the role of NOX in the evolution of ALA in the hamster, a susceptible model. Our study showed that administration of a selective NADPH oxidase 2 (NOX2) enzyme inhibitor significantly decreases the percentage of ALA, the size of inflammatory foci, the number of neutrophils, and NOX activity indicated by the reduction in superoxide anion (O2−) production. Moreover, in vitro, the apocynin damages amoebae. Our results showed that apocynin administration induces a decrease in the activity of NOX that could favor a decrease in ALA progression.</description><subject>Abscesses</subject><subject>Amebiasis</subject><subject>amebic liver abscess</subject><subject>Animal models</subject><subject>apocynin</subject><subject>CYBB protein</subject><subject>Drug dosages</subject><subject>Entamoeba histolytica</subject><subject>Enzyme inhibitors</subject><subject>Enzymes</subject><subject>Gastrointestinal system</subject><subject>Hamsters</subject><subject>Health care</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Laboratory animals</subject><subject>Leukocytes (neutrophilic)</subject><subject>Liver</subject><subject>Liver diseases</subject><subject>Microscopy</subject><subject>NAD(P)H oxidase</subject><subject>NADPH oxidase</subject><subject>neutrophil</subject><subject>Neutrophils</subject><subject>NOX2</subject><subject>Parasites</subject><subject>Parasitic diseases</subject><subject>Photographic industry</subject><subject>Protozoa</subject><subject>Reactive oxygen species</subject><subject>Superoxide anions</subject><subject>Tropical diseases</subject><issn>2227-9059</issn><issn>2227-9059</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1vEzEQXSEQrUr_AQdLXDg0xd8fJ7QqhUSKaA_lbNleb-ooawd7ExF-PV5SAUG1Dx49v3njeZ6meYvgNSEKfrAhDb4LLkRfEIISE4xfNOcYYzFTkKmX_8RnzWUpa1iXQkQi-ro5I4JjLpE8b7612-QOMcQrYCL42n66n4O7H6EzxYPb-PMweLCIj8GGMeUrcJ_93sexgHbwNjiwDHufQWuL86WAEMHcDGX0-U3zqjeb4i-fzovm4fPtw818trz7srhplzPHqBhnxDDnOVF95yQkkFkGJUGS277CynQdoZJhAq1ATmJB-k5SyWGvDKVMcHLRLI6yXTJrvc1hMPmgkwn6N5DySps8BrfxmnDXUcSJRdxR5a2R1jrpbC8p4YawqvXxqLXd2Wqtq21mszkRPb2J4VGv0l4jSBlWaHrN-yeFnL7vfBn1EKoxm42JPu2KxpIJSRlBU7F3_1HXaZdjtWpicUmkUOIva2VqByH2qRZ2k6hu6wdSQYSSlXX9DKvuzg_Bpej7UPGTBHpMcDmVkn3_p0kE9TRd-rnpIr8A9ErBZQ</recordid><startdate>20230801</startdate><enddate>20230801</enddate><creator>Higuera-Martínez, Germán</creator><creator>Arciniega-Martínez, Ivonne Maciel</creator><creator>Jarillo-Luna, Rosa Adriana</creator><creator>Cárdenas-Jaramillo, Luz María</creator><creator>Levaro-Loquio, David</creator><creator>Velásquez-Torres, Maritza</creator><creator>Abarca-Rojano, Edgar</creator><creator>Reséndiz-Albor, Aldo Arturo</creator><creator>Pacheco-Yépez, Judith</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-0467-2528</orcidid><orcidid>https://orcid.org/0000-0003-1415-5524</orcidid><orcidid>https://orcid.org/0000-0001-8648-7734</orcidid><orcidid>https://orcid.org/0000-0001-5250-7952</orcidid><orcidid>https://orcid.org/0000-0002-0807-7104</orcidid><orcidid>https://orcid.org/0000-0003-0283-1812</orcidid></search><sort><creationdate>20230801</creationdate><title>Apocynin, an NADPH Oxidase Enzyme Inhibitor, Prevents Amebic Liver Abscess in Hamster</title><author>Higuera-Martínez, Germán ; Arciniega-Martínez, Ivonne Maciel ; Jarillo-Luna, Rosa Adriana ; Cárdenas-Jaramillo, Luz María ; Levaro-Loquio, David ; Velásquez-Torres, Maritza ; Abarca-Rojano, Edgar ; Reséndiz-Albor, Aldo Arturo ; Pacheco-Yépez, Judith</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c547t-3a5ce639fdc80305b5083186bfce69add3485230b71c8273fd84860f9a445763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Abscesses</topic><topic>Amebiasis</topic><topic>amebic liver abscess</topic><topic>Animal models</topic><topic>apocynin</topic><topic>CYBB protein</topic><topic>Drug dosages</topic><topic>Entamoeba histolytica</topic><topic>Enzyme inhibitors</topic><topic>Enzymes</topic><topic>Gastrointestinal system</topic><topic>Hamsters</topic><topic>Health care</topic><topic>Infections</topic><topic>Inflammation</topic><topic>Laboratory animals</topic><topic>Leukocytes (neutrophilic)</topic><topic>Liver</topic><topic>Liver diseases</topic><topic>Microscopy</topic><topic>NAD(P)H oxidase</topic><topic>NADPH oxidase</topic><topic>neutrophil</topic><topic>Neutrophils</topic><topic>NOX2</topic><topic>Parasites</topic><topic>Parasitic diseases</topic><topic>Photographic industry</topic><topic>Protozoa</topic><topic>Reactive oxygen species</topic><topic>Superoxide anions</topic><topic>Tropical diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Higuera-Martínez, Germán</creatorcontrib><creatorcontrib>Arciniega-Martínez, Ivonne Maciel</creatorcontrib><creatorcontrib>Jarillo-Luna, Rosa Adriana</creatorcontrib><creatorcontrib>Cárdenas-Jaramillo, Luz María</creatorcontrib><creatorcontrib>Levaro-Loquio, David</creatorcontrib><creatorcontrib>Velásquez-Torres, Maritza</creatorcontrib><creatorcontrib>Abarca-Rojano, Edgar</creatorcontrib><creatorcontrib>Reséndiz-Albor, Aldo Arturo</creatorcontrib><creatorcontrib>Pacheco-Yépez, Judith</creatorcontrib><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>ProQuest Biological Science Journals</collection><collection>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Biomedicines</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Higuera-Martínez, Germán</au><au>Arciniega-Martínez, Ivonne Maciel</au><au>Jarillo-Luna, Rosa Adriana</au><au>Cárdenas-Jaramillo, Luz María</au><au>Levaro-Loquio, David</au><au>Velásquez-Torres, Maritza</au><au>Abarca-Rojano, Edgar</au><au>Reséndiz-Albor, Aldo Arturo</au><au>Pacheco-Yépez, Judith</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Apocynin, an NADPH Oxidase Enzyme Inhibitor, Prevents Amebic Liver Abscess in Hamster</atitle><jtitle>Biomedicines</jtitle><date>2023-08-01</date><risdate>2023</risdate><volume>11</volume><issue>8</issue><spage>2322</spage><pages>2322-</pages><issn>2227-9059</issn><eissn>2227-9059</eissn><abstract>Amebiasis is an intestinal infection caused by Entamoeba histolytica. Amebic liver abscess (ALA) is the most common extraintestinal complication of amebiasis. In animal models of ALA, neutrophils have been shown to be the first cells to come into contact with Entamoeba histolytica during the initial phase of ALA. One of the multiple mechanisms by which neutrophils exhibit amebicidal activity is through reactive oxygen species (ROS) and the enzyme NADPH oxidase (NOX2), which generates and transports electrons to subsequently reduce molecular oxygen into superoxide anion. Previous reports have shown that ROS release in the susceptible animal species (hamster) is mainly stimulated by the pathogen, in turn provoking such an exacerbated inflammatory reaction that it is unable to be controlled and results in the death of the animal model. Apocynin is a natural inhibitor of NADPH oxidase. No information is available on the role of NOX in the evolution of ALA in the hamster, a susceptible model. Our study showed that administration of a selective NADPH oxidase 2 (NOX2) enzyme inhibitor significantly decreases the percentage of ALA, the size of inflammatory foci, the number of neutrophils, and NOX activity indicated by the reduction in superoxide anion (O2−) production. Moreover, in vitro, the apocynin damages amoebae. Our results showed that apocynin administration induces a decrease in the activity of NOX that could favor a decrease in ALA progression.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>37626818</pmid><doi>10.3390/biomedicines11082322</doi><orcidid>https://orcid.org/0000-0003-0467-2528</orcidid><orcidid>https://orcid.org/0000-0003-1415-5524</orcidid><orcidid>https://orcid.org/0000-0001-8648-7734</orcidid><orcidid>https://orcid.org/0000-0001-5250-7952</orcidid><orcidid>https://orcid.org/0000-0002-0807-7104</orcidid><orcidid>https://orcid.org/0000-0003-0283-1812</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Abscesses Amebiasis amebic liver abscess Animal models apocynin CYBB protein Drug dosages Entamoeba histolytica Enzyme inhibitors Enzymes Gastrointestinal system Hamsters Health care Infections Inflammation Laboratory animals Leukocytes (neutrophilic) Liver Liver diseases Microscopy NAD(P)H oxidase NADPH oxidase neutrophil Neutrophils NOX2 Parasites Parasitic diseases Photographic industry Protozoa Reactive oxygen species Superoxide anions Tropical diseases |
title | Apocynin, an NADPH Oxidase Enzyme Inhibitor, Prevents Amebic Liver Abscess in Hamster |
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