Citrate Attenuates Adenine-Induced Chronic Renal Failure in Rats by Modulating the Th17/Treg Cell Balance
Citrate is commonly used as an anticoagulant in hemodialysis for chronic renal failure (CRF) and for the regulation of the immune dysfunction in CRF patients. The objective of this study was to investigate the effect of citrate on the balance of T helper 17 (Th17) and regulatory T (Treg) cells in CR...
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Veröffentlicht in: | Inflammation 2016-02, Vol.39 (1), p.79-86 |
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creator | Ou, Yan Li, Shuiqin Zhu, Xiaojing Gui, Baosong Yao, Ganglian Ma, Liqun Zhu, Dan Fu, Rongguo Ge, Heng Wang, Li Jia, Lining Tian, Lifang Duan, Zhaoyang |
description | Citrate is commonly used as an anticoagulant in hemodialysis for chronic renal failure (CRF) and for the regulation of the immune dysfunction in CRF patients. The objective of this study was to investigate the effect of citrate on the balance of T helper 17 (Th17) and regulatory T (Treg) cells in CRF. The levels of blood urea nitrogen (BUN) and serum creatinine (Scr) were significantly increased in the CRF model group compared to the control group, and were decreased in the citrate-treated groups. Citrate treatment inhibited the viability of Th17 cells while elevating the viability of Treg cells in CRF rats. Moreover, Th17-related cytokines significantly decreased while the Treg-related cytokines significantly increased with citrate treatment. Moreover, citrate had a negative influence on the deviation of Th17/Treg cells in CRF rats. Therefore, our study suggests that citrate had an anti-inflammatory effect on CRF through the modulation of the Th17/Treg balance. |
doi_str_mv | 10.1007/s10753-015-0225-y |
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The objective of this study was to investigate the effect of citrate on the balance of T helper 17 (Th17) and regulatory T (Treg) cells in CRF. The levels of blood urea nitrogen (BUN) and serum creatinine (Scr) were significantly increased in the CRF model group compared to the control group, and were decreased in the citrate-treated groups. Citrate treatment inhibited the viability of Th17 cells while elevating the viability of Treg cells in CRF rats. Moreover, Th17-related cytokines significantly decreased while the Treg-related cytokines significantly increased with citrate treatment. Moreover, citrate had a negative influence on the deviation of Th17/Treg cells in CRF rats. Therefore, our study suggests that citrate had an anti-inflammatory effect on CRF through the modulation of the Th17/Treg balance.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-015-0225-y</identifier><identifier>PMID: 26253296</identifier><identifier>CODEN: INFLD4</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adenine - pharmacology ; Animals ; Anti-Inflammatory Agents - therapeutic use ; Biomedical and Life Sciences ; Biomedicine ; Blood Urea Nitrogen ; Cell Survival - drug effects ; Citric Acid - therapeutic use ; Creatinine - blood ; Cytokines - metabolism ; Disease Models, Animal ; Forkhead Transcription Factors - biosynthesis ; Immunology ; Inflammation - drug therapy ; Internal Medicine ; Kidney Failure, Chronic - chemically induced ; Kidney Failure, Chronic - drug therapy ; Nuclear Receptor Subfamily 1, Group F, Member 3 - biosynthesis ; Pathology ; Pharmacology/Toxicology ; Rats ; Rats, Sprague-Dawley ; Rheumatology ; T-Lymphocytes, Regulatory - immunology ; Th17 Cells - immunology</subject><ispartof>Inflammation, 2016-02, Vol.39 (1), p.79-86</ispartof><rights>Springer Science+Business Media New York 2015</rights><rights>Springer Science+Business Media New York 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-136ddeb9d4228a4a82c45f6b5342fedab28286c83cdcb0f7a38aedb45ed4d5553</citedby><cites>FETCH-LOGICAL-c475t-136ddeb9d4228a4a82c45f6b5342fedab28286c83cdcb0f7a38aedb45ed4d5553</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10753-015-0225-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-015-0225-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26253296$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ou, Yan</creatorcontrib><creatorcontrib>Li, Shuiqin</creatorcontrib><creatorcontrib>Zhu, Xiaojing</creatorcontrib><creatorcontrib>Gui, Baosong</creatorcontrib><creatorcontrib>Yao, Ganglian</creatorcontrib><creatorcontrib>Ma, Liqun</creatorcontrib><creatorcontrib>Zhu, Dan</creatorcontrib><creatorcontrib>Fu, Rongguo</creatorcontrib><creatorcontrib>Ge, Heng</creatorcontrib><creatorcontrib>Wang, Li</creatorcontrib><creatorcontrib>Jia, Lining</creatorcontrib><creatorcontrib>Tian, Lifang</creatorcontrib><creatorcontrib>Duan, Zhaoyang</creatorcontrib><title>Citrate Attenuates Adenine-Induced Chronic Renal Failure in Rats by Modulating the Th17/Treg Cell Balance</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>Citrate is commonly used as an anticoagulant in hemodialysis for chronic renal failure (CRF) and for the regulation of the immune dysfunction in CRF patients. The objective of this study was to investigate the effect of citrate on the balance of T helper 17 (Th17) and regulatory T (Treg) cells in CRF. The levels of blood urea nitrogen (BUN) and serum creatinine (Scr) were significantly increased in the CRF model group compared to the control group, and were decreased in the citrate-treated groups. Citrate treatment inhibited the viability of Th17 cells while elevating the viability of Treg cells in CRF rats. Moreover, Th17-related cytokines significantly decreased while the Treg-related cytokines significantly increased with citrate treatment. Moreover, citrate had a negative influence on the deviation of Th17/Treg cells in CRF rats. Therefore, our study suggests that citrate had an anti-inflammatory effect on CRF through the modulation of the Th17/Treg balance.</description><subject>Adenine - pharmacology</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood Urea Nitrogen</subject><subject>Cell Survival - drug effects</subject><subject>Citric Acid - therapeutic use</subject><subject>Creatinine - blood</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Forkhead Transcription Factors - biosynthesis</subject><subject>Immunology</subject><subject>Inflammation - drug therapy</subject><subject>Internal Medicine</subject><subject>Kidney Failure, Chronic - chemically induced</subject><subject>Kidney Failure, Chronic - drug therapy</subject><subject>Nuclear Receptor Subfamily 1, Group F, Member 3 - biosynthesis</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rheumatology</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>Th17 Cells - immunology</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqNkU9rFDEYh4Modm39AF4k4KWX2PydZI7rYG2hIpTtOWSSd3ZTZjM1mTnstzftVpGC4OkNvM_vl5AHoQ-MfmaU6ovCqFaCUKYI5VyRwyu0YkoLwpVuXqMVFQ0lom31CXpXyj2l1LRGvEUnvOFK8LZZodjFObsZ8HqeIS31VPA6QIoJyHUKi4eAu12eUvT4FpIb8aWL45IBx4Rv3Vxwf8Dfp7CMbo5pi-cd4M2O6YtNhi3uYBzxFze65OEMvRncWOD98zxFd5dfN90Vufnx7bpb3xAvtZoJE00I0LdBcm6cdIZ7qYamV0LyAYLrueGm8Ub44Hs6aCeMg9BLBUEGpZQ4RefH3oc8_VygzHYfi68PcQmmpVimG6OMEoL-D6oYk0zJin56gd5PS67_8URJIwQ3baXYkfJ5KiXDYB9y3Lt8sIzaR2X2qMxWZfZRmT3UzMfn5qXfQ_iT-O2oAvwIlLpKW8h_Xf3P1l97GaCB</recordid><startdate>20160201</startdate><enddate>20160201</enddate><creator>Ou, Yan</creator><creator>Li, Shuiqin</creator><creator>Zhu, Xiaojing</creator><creator>Gui, Baosong</creator><creator>Yao, Ganglian</creator><creator>Ma, Liqun</creator><creator>Zhu, Dan</creator><creator>Fu, Rongguo</creator><creator>Ge, Heng</creator><creator>Wang, Li</creator><creator>Jia, Lining</creator><creator>Tian, Lifang</creator><creator>Duan, Zhaoyang</creator><general>Springer US</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>7T5</scope><scope>7TO</scope><scope>7U9</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>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20160201</creationdate><title>Citrate Attenuates Adenine-Induced Chronic Renal Failure in Rats by Modulating the Th17/Treg Cell Balance</title><author>Ou, Yan ; 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The objective of this study was to investigate the effect of citrate on the balance of T helper 17 (Th17) and regulatory T (Treg) cells in CRF. The levels of blood urea nitrogen (BUN) and serum creatinine (Scr) were significantly increased in the CRF model group compared to the control group, and were decreased in the citrate-treated groups. Citrate treatment inhibited the viability of Th17 cells while elevating the viability of Treg cells in CRF rats. Moreover, Th17-related cytokines significantly decreased while the Treg-related cytokines significantly increased with citrate treatment. Moreover, citrate had a negative influence on the deviation of Th17/Treg cells in CRF rats. Therefore, our study suggests that citrate had an anti-inflammatory effect on CRF through the modulation of the Th17/Treg balance.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>26253296</pmid><doi>10.1007/s10753-015-0225-y</doi><tpages>8</tpages></addata></record> |
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subjects | Adenine - pharmacology Animals Anti-Inflammatory Agents - therapeutic use Biomedical and Life Sciences Biomedicine Blood Urea Nitrogen Cell Survival - drug effects Citric Acid - therapeutic use Creatinine - blood Cytokines - metabolism Disease Models, Animal Forkhead Transcription Factors - biosynthesis Immunology Inflammation - drug therapy Internal Medicine Kidney Failure, Chronic - chemically induced Kidney Failure, Chronic - drug therapy Nuclear Receptor Subfamily 1, Group F, Member 3 - biosynthesis Pathology Pharmacology/Toxicology Rats Rats, Sprague-Dawley Rheumatology T-Lymphocytes, Regulatory - immunology Th17 Cells - immunology |
title | Citrate Attenuates Adenine-Induced Chronic Renal Failure in Rats by Modulating the Th17/Treg Cell Balance |
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