Butyrate suppresses atherosclerotic inflammation by regulating macrophages and polarization via GPR43/HDAC-miRNAs axis in ApoE-/- mice
Chronic low-grade inflammation is regarded to an important signature of atherosclerosis (AS). Macrophage (Mψ) and related polarization have been demonstrated to play a crucial role in the occurrence and development of AS inflammation. Butyrate, a bioactive molecule produced by the intestinal flora,...
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| Veröffentlicht in: | PloS one 2023-03, Vol.18 (3), p.e0282685-e0282685 |
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| creator | Ma, Huiyan Yang, Libo Liu, Yajuan Yan, Ru Wang, Rui Zhang, Peng Bai, Zhixia Liu, Yuanyuan Ren, Yi Li, Yiwei Jiang, Xin Wang, Ting Ma, Ping Zhang, Qining Li, Aifei Guo, Mixue Zhang, Xiaoxia Jia, Shaobin Wang, Hao |
| description | Chronic low-grade inflammation is regarded to an important signature of atherosclerosis (AS). Macrophage (Mψ) and related polarization have been demonstrated to play a crucial role in the occurrence and development of AS inflammation. Butyrate, a bioactive molecule produced by the intestinal flora, has been increasingly demonstrated to exhibit a vital role for regulating the inflammation in chronic metabolic diseases. However, the effectiveness and multiple anti-inflammation mechanisms of butyrate on AS still need to be further understood. ApoE-/- mice fed with high-fat diet as AS model were administered with sodium butyrate (NaB) for 14 weeks of treatment. Our results showed that the atherosclerotic lesion in the AS group was dramatically reduced after NaB intervention. Moreover, deteriorated routine parameters of AS including body weights (BWs), low-density lipoprotein (LDL-C), triglyceride (TG), total cholesterol (TC) were significantly reversed by NaB administration. Abnormal elevated plasma and aorta pro-inflammatory indicators including interleukin (IL)-1β, IL-6, IL-17A, tumor necrosis factor (TNF)-α and lipopolysaccharide (LPS), as well as reduced anti-inflammatory IL-10 in plasma were respectively rectified after NaB administration. Consistently, accumulated Mψ and associated imbalance of polarization in the arota were attenuated with NaB treatment. Importantly, we demonstrated that the suppression of Mψ and associated polarization of NaB was dependent on binding G-protein coupled receptor (GPR) and inhibiting histone deacetylase HDAC3. Moreover, we found that intestinal butyrate-producing bacteria, anti-inflammatory bacteria and intestinal tight junction protein zonula occludens-1 (ZO)-1 may contribute to this effectiveness. Intriguingly, according to transcriptome sequencing of atherosclerotic aorta, 29 elevated and 24 reduced miRNAs were found after NaB treatment, especially miR-7a-5p, suggesting that non-coding RNA may possess a potential role in the protection of NaB against AS. Correlation analysis showed that there were close complicated interactions among gut microbiota, inflammation and differential miRNAs. Collectively, this study revealed that dietary NaB may ameliorate atherosclerotic inflammation by regulating Mψ polarization via GPR43/HDAC-miRNAs axis in ApoE-/- mice. |
| doi_str_mv | 10.1371/journal.pone.0282685 |
| format | Article |
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Macrophage (Mψ) and related polarization have been demonstrated to play a crucial role in the occurrence and development of AS inflammation. Butyrate, a bioactive molecule produced by the intestinal flora, has been increasingly demonstrated to exhibit a vital role for regulating the inflammation in chronic metabolic diseases. However, the effectiveness and multiple anti-inflammation mechanisms of butyrate on AS still need to be further understood. ApoE-/- mice fed with high-fat diet as AS model were administered with sodium butyrate (NaB) for 14 weeks of treatment. Our results showed that the atherosclerotic lesion in the AS group was dramatically reduced after NaB intervention. Moreover, deteriorated routine parameters of AS including body weights (BWs), low-density lipoprotein (LDL-C), triglyceride (TG), total cholesterol (TC) were significantly reversed by NaB administration. Abnormal elevated plasma and aorta pro-inflammatory indicators including interleukin (IL)-1β, IL-6, IL-17A, tumor necrosis factor (TNF)-α and lipopolysaccharide (LPS), as well as reduced anti-inflammatory IL-10 in plasma were respectively rectified after NaB administration. Consistently, accumulated Mψ and associated imbalance of polarization in the arota were attenuated with NaB treatment. Importantly, we demonstrated that the suppression of Mψ and associated polarization of NaB was dependent on binding G-protein coupled receptor (GPR) and inhibiting histone deacetylase HDAC3. Moreover, we found that intestinal butyrate-producing bacteria, anti-inflammatory bacteria and intestinal tight junction protein zonula occludens-1 (ZO)-1 may contribute to this effectiveness. Intriguingly, according to transcriptome sequencing of atherosclerotic aorta, 29 elevated and 24 reduced miRNAs were found after NaB treatment, especially miR-7a-5p, suggesting that non-coding RNA may possess a potential role in the protection of NaB against AS. Correlation analysis showed that there were close complicated interactions among gut microbiota, inflammation and differential miRNAs. Collectively, this study revealed that dietary NaB may ameliorate atherosclerotic inflammation by regulating Mψ polarization via GPR43/HDAC-miRNAs axis in ApoE-/- mice.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0282685</identifier><identifier>PMID: 36888629</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Antibodies ; Aorta ; Apolipoprotein E ; Apolipoproteins E - genetics ; Apolipoproteins E - metabolism ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - metabolism ; Bacteria ; Biology and Life Sciences ; Butyric Acid - metabolism ; Butyric Acid - pharmacology ; Cholesterol ; Correlation analysis ; Cytokines ; Diet ; Effectiveness ; Flora ; G protein-coupled receptors ; High density lipoprotein ; High fat diet ; Histone deacetylase ; Inflammation ; Interleukin ; Interleukin 10 ; Interleukin 6 ; Intestinal microflora ; Intestine ; Laboratory animals ; Lipopolysaccharides ; Lipoproteins ; Low density lipoprotein ; Macrophages ; Macrophages - metabolism ; Medical laboratories ; Medical research ; Medicine and Health Sciences ; Metabolic disorders ; Metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout, ApoE ; Microbiota ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Plasma ; Polarization ; Proteins ; Sodium ; Sodium butyrate ; Transcriptomes ; Triglycerides ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Zonula occludens-1 protein</subject><ispartof>PloS one, 2023-03, Vol.18 (3), p.e0282685-e0282685</ispartof><rights>Copyright: © 2023 Ma et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</rights><rights>2023 Ma et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 Ma et al 2023 Ma et al</rights><rights>2023 Ma et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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-c526t-1ab6442d44a4cb05c42d37c85c78c1c454f8532beaec214a97f20274563f569d3</citedby><cites>FETCH-LOGICAL-c526t-1ab6442d44a4cb05c42d37c85c78c1c454f8532beaec214a97f20274563f569d3</cites><orcidid>0000-0002-8545-1067</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9994734/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9994734/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36888629$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Huiyan</creatorcontrib><creatorcontrib>Yang, Libo</creatorcontrib><creatorcontrib>Liu, Yajuan</creatorcontrib><creatorcontrib>Yan, Ru</creatorcontrib><creatorcontrib>Wang, Rui</creatorcontrib><creatorcontrib>Zhang, Peng</creatorcontrib><creatorcontrib>Bai, Zhixia</creatorcontrib><creatorcontrib>Liu, Yuanyuan</creatorcontrib><creatorcontrib>Ren, Yi</creatorcontrib><creatorcontrib>Li, Yiwei</creatorcontrib><creatorcontrib>Jiang, Xin</creatorcontrib><creatorcontrib>Wang, Ting</creatorcontrib><creatorcontrib>Ma, Ping</creatorcontrib><creatorcontrib>Zhang, Qining</creatorcontrib><creatorcontrib>Li, Aifei</creatorcontrib><creatorcontrib>Guo, Mixue</creatorcontrib><creatorcontrib>Zhang, Xiaoxia</creatorcontrib><creatorcontrib>Jia, Shaobin</creatorcontrib><creatorcontrib>Wang, Hao</creatorcontrib><title>Butyrate suppresses atherosclerotic inflammation by regulating macrophages and polarization via GPR43/HDAC-miRNAs axis in ApoE-/- mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Chronic low-grade inflammation is regarded to an important signature of atherosclerosis (AS). Macrophage (Mψ) and related polarization have been demonstrated to play a crucial role in the occurrence and development of AS inflammation. Butyrate, a bioactive molecule produced by the intestinal flora, has been increasingly demonstrated to exhibit a vital role for regulating the inflammation in chronic metabolic diseases. However, the effectiveness and multiple anti-inflammation mechanisms of butyrate on AS still need to be further understood. ApoE-/- mice fed with high-fat diet as AS model were administered with sodium butyrate (NaB) for 14 weeks of treatment. Our results showed that the atherosclerotic lesion in the AS group was dramatically reduced after NaB intervention. Moreover, deteriorated routine parameters of AS including body weights (BWs), low-density lipoprotein (LDL-C), triglyceride (TG), total cholesterol (TC) were significantly reversed by NaB administration. Abnormal elevated plasma and aorta pro-inflammatory indicators including interleukin (IL)-1β, IL-6, IL-17A, tumor necrosis factor (TNF)-α and lipopolysaccharide (LPS), as well as reduced anti-inflammatory IL-10 in plasma were respectively rectified after NaB administration. Consistently, accumulated Mψ and associated imbalance of polarization in the arota were attenuated with NaB treatment. Importantly, we demonstrated that the suppression of Mψ and associated polarization of NaB was dependent on binding G-protein coupled receptor (GPR) and inhibiting histone deacetylase HDAC3. Moreover, we found that intestinal butyrate-producing bacteria, anti-inflammatory bacteria and intestinal tight junction protein zonula occludens-1 (ZO)-1 may contribute to this effectiveness. Intriguingly, according to transcriptome sequencing of atherosclerotic aorta, 29 elevated and 24 reduced miRNAs were found after NaB treatment, especially miR-7a-5p, suggesting that non-coding RNA may possess a potential role in the protection of NaB against AS. Correlation analysis showed that there were close complicated interactions among gut microbiota, inflammation and differential miRNAs. Collectively, this study revealed that dietary NaB may ameliorate atherosclerotic inflammation by regulating Mψ polarization via GPR43/HDAC-miRNAs axis in ApoE-/- mice.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Aorta</subject><subject>Apolipoprotein E</subject><subject>Apolipoproteins E - genetics</subject><subject>Apolipoproteins E - metabolism</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - metabolism</subject><subject>Bacteria</subject><subject>Biology and Life Sciences</subject><subject>Butyric Acid - metabolism</subject><subject>Butyric Acid - pharmacology</subject><subject>Cholesterol</subject><subject>Correlation analysis</subject><subject>Cytokines</subject><subject>Diet</subject><subject>Effectiveness</subject><subject>Flora</subject><subject>G protein-coupled receptors</subject><subject>High density lipoprotein</subject><subject>High fat diet</subject><subject>Histone deacetylase</subject><subject>Inflammation</subject><subject>Interleukin</subject><subject>Interleukin 10</subject><subject>Interleukin 6</subject><subject>Intestinal microflora</subject><subject>Intestine</subject><subject>Laboratory animals</subject><subject>Lipopolysaccharides</subject><subject>Lipoproteins</subject><subject>Low density lipoprotein</subject><subject>Macrophages</subject><subject>Macrophages - metabolism</subject><subject>Medical laboratories</subject><subject>Medical research</subject><subject>Medicine and Health Sciences</subject><subject>Metabolic disorders</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout, ApoE</subject><subject>Microbiota</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Plasma</subject><subject>Polarization</subject><subject>Proteins</subject><subject>Sodium</subject><subject>Sodium butyrate</subject><subject>Transcriptomes</subject><subject>Triglycerides</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Zonula occludens-1 protein</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1v1DAQjRCIlsI_QBCJC5fsxp-xL0jLUtpKFaAKztbEcXZdOXFqJxXLD-B342XTqkVc7Bn7veeZ8cuy16hcIFKh5bWfQg9uMfjeLEosMBfsSXaMJMEFxyV5-iA-yl7EeF2WjAjOn2dHhAshOJbH2e-P07gLMJo8TsMQTIwm5jBuTfBRu7SOVue2bx10HYzW93m9y4PZTC5l_SbvQAc_bGGzp_VNPngHwf46QG8t5GffrihZnn9arYvOXn1ZJdhPG5Nkvhr8abEs8s5q8zJ71oKL5tW8n2Q_Pp9-X58Xl1_PLtary0IzzMcCQc0pxQ2lQHVdMp1iUmnBdCU00pTRVjCCawNGY0RBVi0ucUUZJy3jsiEn2duD7uB8VPMIo8KVoAJVlRAJcXFANB6u1RBsB2GnPFj198CHjYKQhuKMqpHUJafcpLIoiEbS1pRYSqFxI1CLktaH-bWp7kyjTT8GcI9EH9_0dqs2_lZJKWlFaBJ4PwsEfzOZOKrORm2cg974aa6bMEZ4gr77B_r_7ugBlX4txmDa-2JQqfa2umOpva3UbKtEe_OwkXvSnY_IHy9bzIU</recordid><startdate>20230308</startdate><enddate>20230308</enddate><creator>Ma, Huiyan</creator><creator>Yang, Libo</creator><creator>Liu, Yajuan</creator><creator>Yan, Ru</creator><creator>Wang, Rui</creator><creator>Zhang, Peng</creator><creator>Bai, Zhixia</creator><creator>Liu, Yuanyuan</creator><creator>Ren, Yi</creator><creator>Li, Yiwei</creator><creator>Jiang, Xin</creator><creator>Wang, Ting</creator><creator>Ma, Ping</creator><creator>Zhang, Qining</creator><creator>Li, Aifei</creator><creator>Guo, Mixue</creator><creator>Zhang, Xiaoxia</creator><creator>Jia, Shaobin</creator><creator>Wang, Hao</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-8545-1067</orcidid></search><sort><creationdate>20230308</creationdate><title>Butyrate suppresses atherosclerotic inflammation by regulating macrophages and polarization via GPR43/HDAC-miRNAs axis in ApoE-/- mice</title><author>Ma, Huiyan ; Yang, Libo ; Liu, Yajuan ; Yan, Ru ; Wang, Rui ; Zhang, Peng ; Bai, Zhixia ; Liu, Yuanyuan ; Ren, Yi ; Li, Yiwei ; Jiang, Xin ; Wang, Ting ; Ma, Ping ; Zhang, Qining ; Li, Aifei ; Guo, Mixue ; Zhang, Xiaoxia ; Jia, Shaobin ; Wang, Hao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-1ab6442d44a4cb05c42d37c85c78c1c454f8532beaec214a97f20274563f569d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Aorta</topic><topic>Apolipoprotein E</topic><topic>Apolipoproteins E - 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genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Plasma</topic><topic>Polarization</topic><topic>Proteins</topic><topic>Sodium</topic><topic>Sodium butyrate</topic><topic>Transcriptomes</topic><topic>Triglycerides</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><topic>Zonula occludens-1 protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Huiyan</creatorcontrib><creatorcontrib>Yang, Libo</creatorcontrib><creatorcontrib>Liu, Yajuan</creatorcontrib><creatorcontrib>Yan, Ru</creatorcontrib><creatorcontrib>Wang, Rui</creatorcontrib><creatorcontrib>Zhang, Peng</creatorcontrib><creatorcontrib>Bai, Zhixia</creatorcontrib><creatorcontrib>Liu, Yuanyuan</creatorcontrib><creatorcontrib>Ren, Yi</creatorcontrib><creatorcontrib>Li, Yiwei</creatorcontrib><creatorcontrib>Jiang, Xin</creatorcontrib><creatorcontrib>Wang, Ting</creatorcontrib><creatorcontrib>Ma, Ping</creatorcontrib><creatorcontrib>Zhang, Qining</creatorcontrib><creatorcontrib>Li, Aifei</creatorcontrib><creatorcontrib>Guo, Mixue</creatorcontrib><creatorcontrib>Zhang, Xiaoxia</creatorcontrib><creatorcontrib>Jia, Shaobin</creatorcontrib><creatorcontrib>Wang, Hao</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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection (ProQuest)</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Huiyan</au><au>Yang, Libo</au><au>Liu, Yajuan</au><au>Yan, Ru</au><au>Wang, Rui</au><au>Zhang, Peng</au><au>Bai, Zhixia</au><au>Liu, Yuanyuan</au><au>Ren, Yi</au><au>Li, Yiwei</au><au>Jiang, Xin</au><au>Wang, Ting</au><au>Ma, Ping</au><au>Zhang, Qining</au><au>Li, Aifei</au><au>Guo, Mixue</au><au>Zhang, Xiaoxia</au><au>Jia, Shaobin</au><au>Wang, Hao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Butyrate suppresses atherosclerotic inflammation by regulating macrophages and polarization via GPR43/HDAC-miRNAs axis in ApoE-/- mice</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2023-03-08</date><risdate>2023</risdate><volume>18</volume><issue>3</issue><spage>e0282685</spage><epage>e0282685</epage><pages>e0282685-e0282685</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Chronic low-grade inflammation is regarded to an important signature of atherosclerosis (AS). Macrophage (Mψ) and related polarization have been demonstrated to play a crucial role in the occurrence and development of AS inflammation. Butyrate, a bioactive molecule produced by the intestinal flora, has been increasingly demonstrated to exhibit a vital role for regulating the inflammation in chronic metabolic diseases. However, the effectiveness and multiple anti-inflammation mechanisms of butyrate on AS still need to be further understood. ApoE-/- mice fed with high-fat diet as AS model were administered with sodium butyrate (NaB) for 14 weeks of treatment. Our results showed that the atherosclerotic lesion in the AS group was dramatically reduced after NaB intervention. Moreover, deteriorated routine parameters of AS including body weights (BWs), low-density lipoprotein (LDL-C), triglyceride (TG), total cholesterol (TC) were significantly reversed by NaB administration. Abnormal elevated plasma and aorta pro-inflammatory indicators including interleukin (IL)-1β, IL-6, IL-17A, tumor necrosis factor (TNF)-α and lipopolysaccharide (LPS), as well as reduced anti-inflammatory IL-10 in plasma were respectively rectified after NaB administration. Consistently, accumulated Mψ and associated imbalance of polarization in the arota were attenuated with NaB treatment. Importantly, we demonstrated that the suppression of Mψ and associated polarization of NaB was dependent on binding G-protein coupled receptor (GPR) and inhibiting histone deacetylase HDAC3. Moreover, we found that intestinal butyrate-producing bacteria, anti-inflammatory bacteria and intestinal tight junction protein zonula occludens-1 (ZO)-1 may contribute to this effectiveness. Intriguingly, according to transcriptome sequencing of atherosclerotic aorta, 29 elevated and 24 reduced miRNAs were found after NaB treatment, especially miR-7a-5p, suggesting that non-coding RNA may possess a potential role in the protection of NaB against AS. Correlation analysis showed that there were close complicated interactions among gut microbiota, inflammation and differential miRNAs. Collectively, this study revealed that dietary NaB may ameliorate atherosclerotic inflammation by regulating Mψ polarization via GPR43/HDAC-miRNAs axis in ApoE-/- mice.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>36888629</pmid><doi>10.1371/journal.pone.0282685</doi><orcidid>https://orcid.org/0000-0002-8545-1067</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2023-03, Vol.18 (3), p.e0282685-e0282685 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2784817788 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animals Antibodies Aorta Apolipoprotein E Apolipoproteins E - genetics Apolipoproteins E - metabolism Arteriosclerosis Atherosclerosis Atherosclerosis - metabolism Bacteria Biology and Life Sciences Butyric Acid - metabolism Butyric Acid - pharmacology Cholesterol Correlation analysis Cytokines Diet Effectiveness Flora G protein-coupled receptors High density lipoprotein High fat diet Histone deacetylase Inflammation Interleukin Interleukin 10 Interleukin 6 Intestinal microflora Intestine Laboratory animals Lipopolysaccharides Lipoproteins Low density lipoprotein Macrophages Macrophages - metabolism Medical laboratories Medical research Medicine and Health Sciences Metabolic disorders Metabolism Mice Mice, Inbred C57BL Mice, Knockout, ApoE Microbiota MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism Plasma Polarization Proteins Sodium Sodium butyrate Transcriptomes Triglycerides Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Zonula occludens-1 protein |
| title | Butyrate suppresses atherosclerotic inflammation by regulating macrophages and polarization via GPR43/HDAC-miRNAs axis in ApoE-/- mice |
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