Function of capric acid in cyclophosphamide-induced intestinal inflammation, oxidative stress, and barrier function in pigs
The small intestine is not only critical for nutrient absorption, but also serves as an important immune organ. Medium-chain fatty acids have nutritional and metabolic effects and support the integrity of the intestinal epithelium. However, their roles in intestinal immunity in pigs are not fully un...
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| description | The small intestine is not only critical for nutrient absorption, but also serves as an important immune organ. Medium-chain fatty acids have nutritional and metabolic effects and support the integrity of the intestinal epithelium. However, their roles in intestinal immunity in pigs are not fully understood. We investigated the effects of a medium-chain fatty acid, capric acid, on intestinal oxidative stress, inflammation, and barrier function in porcine epithelial cells and miniature pigs after treatment with the immune suppressant cyclophosphamide. Capric acid alleviated inflammatory cytokine production (TNF-α and IL-6) and related gene expression (
NF-κB
,
TNF-α
,
IFN-γ
), alleviated oxidative stress (GSSG/GSH ratio, H
2
O
2
, and malondialdehyde), and increased oxidative stress-related gene expression (
SOD1
and
GCLC
) in cyclophosphamide-treated IPEC-J2 cells. The permeability of FD-4 and expression of
ZO-1
and
OCLN
in cyclophosphamide-treated IPEC-J2 cells were reduced by capric acid. Dietary capric acid reduced TNF-α, IL-6, and MDA levels and increased SOD, GPx, and the expression of genes related to pro-inflammatory, oxidative stress, and intestinal barrier functions in cyclophosphamide-treated miniature pigs. These results revealed that capric acid has protective effects against cyclophosphamide-induced small intestinal dysfunction in pigs. |
| doi_str_mv | 10.1038/s41598-017-16561-5 |
| format | Article |
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NF-κB
,
TNF-α
,
IFN-γ
), alleviated oxidative stress (GSSG/GSH ratio, H
2
O
2
, and malondialdehyde), and increased oxidative stress-related gene expression (
SOD1
and
GCLC
) in cyclophosphamide-treated IPEC-J2 cells. The permeability of FD-4 and expression of
ZO-1
and
OCLN
in cyclophosphamide-treated IPEC-J2 cells were reduced by capric acid. Dietary capric acid reduced TNF-α, IL-6, and MDA levels and increased SOD, GPx, and the expression of genes related to pro-inflammatory, oxidative stress, and intestinal barrier functions in cyclophosphamide-treated miniature pigs. These results revealed that capric acid has protective effects against cyclophosphamide-induced small intestinal dysfunction in pigs.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-017-16561-5</identifier><identifier>PMID: 29184078</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>38/77 ; 631/601/1737 ; 692/4020/2199 ; Cyclophosphamide ; Epithelial cells ; Epithelium ; Fatty acids ; Gene expression ; Humanities and Social Sciences ; Hydrogen peroxide ; Inflammation ; Interferon ; Interleukin 6 ; Malondialdehyde ; multidisciplinary ; NF-κB protein ; Oxidative stress ; Permeability ; Science ; Science (multidisciplinary) ; Small intestine ; Superoxide dismutase ; Swine ; Tumor necrosis factor-α ; Zonula occludens-1 protein ; γ-Interferon</subject><ispartof>Scientific reports, 2017-11, Vol.7 (1), p.16530-12, Article 16530</ispartof><rights>The Author(s) 2017</rights><rights>2017. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c540t-9ab09080f951ebb45f8efba8c33049a9a2608d15e93f890d2f44015fcc9d98153</citedby><cites>FETCH-LOGICAL-c540t-9ab09080f951ebb45f8efba8c33049a9a2608d15e93f890d2f44015fcc9d98153</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/PMC5705592/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5705592/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29184078$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Sang In</creatorcontrib><creatorcontrib>Kang, Kyung Soo</creatorcontrib><title>Function of capric acid in cyclophosphamide-induced intestinal inflammation, oxidative stress, and barrier function in pigs</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>The small intestine is not only critical for nutrient absorption, but also serves as an important immune organ. Medium-chain fatty acids have nutritional and metabolic effects and support the integrity of the intestinal epithelium. However, their roles in intestinal immunity in pigs are not fully understood. We investigated the effects of a medium-chain fatty acid, capric acid, on intestinal oxidative stress, inflammation, and barrier function in porcine epithelial cells and miniature pigs after treatment with the immune suppressant cyclophosphamide. Capric acid alleviated inflammatory cytokine production (TNF-α and IL-6) and related gene expression (
NF-κB
,
TNF-α
,
IFN-γ
), alleviated oxidative stress (GSSG/GSH ratio, H
2
O
2
, and malondialdehyde), and increased oxidative stress-related gene expression (
SOD1
and
GCLC
) in cyclophosphamide-treated IPEC-J2 cells. The permeability of FD-4 and expression of
ZO-1
and
OCLN
in cyclophosphamide-treated IPEC-J2 cells were reduced by capric acid. Dietary capric acid reduced TNF-α, IL-6, and MDA levels and increased SOD, GPx, and the expression of genes related to pro-inflammatory, oxidative stress, and intestinal barrier functions in cyclophosphamide-treated miniature pigs. These results revealed that capric acid has protective effects against cyclophosphamide-induced small intestinal dysfunction in pigs.</description><subject>38/77</subject><subject>631/601/1737</subject><subject>692/4020/2199</subject><subject>Cyclophosphamide</subject><subject>Epithelial cells</subject><subject>Epithelium</subject><subject>Fatty acids</subject><subject>Gene expression</subject><subject>Humanities and Social Sciences</subject><subject>Hydrogen peroxide</subject><subject>Inflammation</subject><subject>Interferon</subject><subject>Interleukin 6</subject><subject>Malondialdehyde</subject><subject>multidisciplinary</subject><subject>NF-κB protein</subject><subject>Oxidative stress</subject><subject>Permeability</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Small intestine</subject><subject>Superoxide dismutase</subject><subject>Swine</subject><subject>Tumor necrosis factor-α</subject><subject>Zonula occludens-1 protein</subject><subject>γ-Interferon</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kU9rFTEUxYMottR-ARcScOOiozeZZCbZCFKsCgU3ug6Z_HkvZSYZk5li8cub8bXlKZhNLtxfzr0nB6GXBN4SaMW7wgiXogHSN6TjHWn4E3RKgfGGtpQ-PapP0HkpN1APp5IR-RydUEkEg16col9XazRLSBEnj42eczBYm2BxiNjcmTHN-1TmvZ6CdU2IdjVu6y2uLCHqsZZ-1NOkN4kLnH4GW8tbh8uSXSkXWEeLB51zcBn7h1FVew678gI983os7vz-PkPfrz5-u_zcXH_99OXyw3VjOIOlkXoACQK85MQNA-NeOD9oYdoWmNRS0w6EJdzJ1gsJlnrGgHBvjLRSEN6eofcH3XkdJmeNi0vWo6peJ53vVNJB_d2JYa926VbxHjiXtAq8uRfI6cdaraspFOPGUUeX1qKI7IH2NZWuoq__QW_SmutPbVQnJTAm-0rRA2VyKiU7_7gMAbXFqw7xqhqv-hOv2my8Orbx-OQhzAq0B6DUVty5fDT7_7K_AfiHstg</recordid><startdate>20171128</startdate><enddate>20171128</enddate><creator>Lee, Sang In</creator><creator>Kang, Kyung Soo</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20171128</creationdate><title>Function of capric acid in cyclophosphamide-induced intestinal inflammation, oxidative stress, and barrier function in pigs</title><author>Lee, Sang In ; Kang, Kyung Soo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-9ab09080f951ebb45f8efba8c33049a9a2608d15e93f890d2f44015fcc9d98153</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>38/77</topic><topic>631/601/1737</topic><topic>692/4020/2199</topic><topic>Cyclophosphamide</topic><topic>Epithelial cells</topic><topic>Epithelium</topic><topic>Fatty acids</topic><topic>Gene expression</topic><topic>Humanities and Social Sciences</topic><topic>Hydrogen peroxide</topic><topic>Inflammation</topic><topic>Interferon</topic><topic>Interleukin 6</topic><topic>Malondialdehyde</topic><topic>multidisciplinary</topic><topic>NF-κB protein</topic><topic>Oxidative stress</topic><topic>Permeability</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Small intestine</topic><topic>Superoxide dismutase</topic><topic>Swine</topic><topic>Tumor necrosis factor-α</topic><topic>Zonula occludens-1 protein</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Sang In</creatorcontrib><creatorcontrib>Kang, Kyung Soo</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science 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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Sang In</au><au>Kang, Kyung Soo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Function of capric acid in cyclophosphamide-induced intestinal inflammation, oxidative stress, and barrier function in pigs</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2017-11-28</date><risdate>2017</risdate><volume>7</volume><issue>1</issue><spage>16530</spage><epage>12</epage><pages>16530-12</pages><artnum>16530</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>The small intestine is not only critical for nutrient absorption, but also serves as an important immune organ. Medium-chain fatty acids have nutritional and metabolic effects and support the integrity of the intestinal epithelium. However, their roles in intestinal immunity in pigs are not fully understood. We investigated the effects of a medium-chain fatty acid, capric acid, on intestinal oxidative stress, inflammation, and barrier function in porcine epithelial cells and miniature pigs after treatment with the immune suppressant cyclophosphamide. Capric acid alleviated inflammatory cytokine production (TNF-α and IL-6) and related gene expression (
NF-κB
,
TNF-α
,
IFN-γ
), alleviated oxidative stress (GSSG/GSH ratio, H
2
O
2
, and malondialdehyde), and increased oxidative stress-related gene expression (
SOD1
and
GCLC
) in cyclophosphamide-treated IPEC-J2 cells. The permeability of FD-4 and expression of
ZO-1
and
OCLN
in cyclophosphamide-treated IPEC-J2 cells were reduced by capric acid. Dietary capric acid reduced TNF-α, IL-6, and MDA levels and increased SOD, GPx, and the expression of genes related to pro-inflammatory, oxidative stress, and intestinal barrier functions in cyclophosphamide-treated miniature pigs. These results revealed that capric acid has protective effects against cyclophosphamide-induced small intestinal dysfunction in pigs.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29184078</pmid><doi>10.1038/s41598-017-16561-5</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 38/77 631/601/1737 692/4020/2199 Cyclophosphamide Epithelial cells Epithelium Fatty acids Gene expression Humanities and Social Sciences Hydrogen peroxide Inflammation Interferon Interleukin 6 Malondialdehyde multidisciplinary NF-κB protein Oxidative stress Permeability Science Science (multidisciplinary) Small intestine Superoxide dismutase Swine Tumor necrosis factor-α Zonula occludens-1 protein γ-Interferon |
| title | Function of capric acid in cyclophosphamide-induced intestinal inflammation, oxidative stress, and barrier function in pigs |
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