DHA protects against monosodium urate-induced inflammation through modulation of oxidative stress
Acute gouty inflammation could be triggered by phagocytosis of monosodium urate (MSU) by immune cells. This study investigated the protective effect and underlying mechanism of docosahexaenoic acid (DHA) on MSU-induced inflammation in vitro and in vivo . Results showed that DHA effectively inhibited...
Gespeichert in:
| Veröffentlicht in: | Food & function 2019-07, Vol.1 (7), p.41-421 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 421 |
|---|---|
| container_issue | 7 |
| container_start_page | 41 |
| container_title | Food & function |
| container_volume | 1 |
| creator | Zhang, Yue Liu, Lu Sun, Dongzhe He, Yongjing Jiang, Yue Cheng, Ka-Wing Chen, Feng |
| description | Acute gouty inflammation could be triggered by phagocytosis of monosodium urate (MSU) by immune cells. This study investigated the protective effect and underlying mechanism of docosahexaenoic acid (DHA) on MSU-induced inflammation
in vitro
and
in vivo
. Results showed that DHA effectively inhibited MSU-induced expression and secretion of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in THP-1 cells. Intracellular reactive oxygen species (ROS) production triggered by MSU was alleviated by DHA treatment. Furthermore, DHA promoted the nuclear translocation of nuclear factor E2-related factor 2 (Nrf2), wherein Nrf2 further mediated the expression of multiple antioxidant enzymes such as, heme oxygenase-1 (HO-1), NAD(P)H: quinone oxidoreductase-1 (NQO1) and catalase, which are closely related with redox homeostasis. DHA treatment also restored MSU-induced impairment of mitochondrial transmembrane potential. In addition, oral administration of DHA-rich microalgal oil to C57BL/6 mice effectively reduced the infiltration of neutrophils, and decreased the expression and secretion of inflammatory cytokines. Altogether, our results suggest that DHA or DHA-rich microalgal oil may be a promising natural agent for the prevention of MSU-induced inflammation and potentially acute gout at least partly by attenuating oxidative stress.
DHA and DHA-rich microalgal oil protect against monosodium urate-induced inflammation
via
regulating oxidative stress and inhibiting NLRP3-mediated inflammatory cytokine secretion. |
| doi_str_mv | 10.1039/c9fo00573k |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1039_C9FO00573K</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2243489703</sourcerecordid><originalsourceid>FETCH-LOGICAL-c378t-ea1cbe608f2d34cbe5dc8893637192a9c84009e46dd206b4d31e489ad1bbb9b83</originalsourceid><addsrcrecordid>eNpdkc9LwzAUx4MobsxdvCsFLyJUkyZtk-OYzomDXRS8lTRJt862mfkh-t-buR-C75L38j7vy8s3AJwjeIsgZneCVRrCNMfvR6CfQJLEWQrfjvc5YVkPDK1dwRCYMcroKehhlCCS5bAP-P10FK2Ndko4G_EFrzvrolZ32mpZ-zbyhjsV1530Qsmo7qqGty13te4itzTaL5aBlr7ZXukq0l-1DMWniqwzytozcFLxxqrh7hyA18nDy3gaz-aPT-PRLBY4py5WHIlSZZBWicQkpKkUlDKc4RyxhDNBCYRMkUzKBGYlkRgpQhmXqCxLVlI8ANdb3fCaD6-sK9raCtU0vFPa2yJJCA4DOcQBvfqHrrQ3XdguUCnNc5pmG8GbLSWMttaoqlibuuXmu0Cw2HhfjNlk_uv9c4Avd5K-bJU8oHunA3CxBYwVh-7f5-EfI3aJzw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2258778568</pqid></control><display><type>article</type><title>DHA protects against monosodium urate-induced inflammation through modulation of oxidative stress</title><source>MEDLINE</source><source>Royal Society Of Chemistry Journals 2008-</source><creator>Zhang, Yue ; Liu, Lu ; Sun, Dongzhe ; He, Yongjing ; Jiang, Yue ; Cheng, Ka-Wing ; Chen, Feng</creator><creatorcontrib>Zhang, Yue ; Liu, Lu ; Sun, Dongzhe ; He, Yongjing ; Jiang, Yue ; Cheng, Ka-Wing ; Chen, Feng</creatorcontrib><description>Acute gouty inflammation could be triggered by phagocytosis of monosodium urate (MSU) by immune cells. This study investigated the protective effect and underlying mechanism of docosahexaenoic acid (DHA) on MSU-induced inflammation
in vitro
and
in vivo
. Results showed that DHA effectively inhibited MSU-induced expression and secretion of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in THP-1 cells. Intracellular reactive oxygen species (ROS) production triggered by MSU was alleviated by DHA treatment. Furthermore, DHA promoted the nuclear translocation of nuclear factor E2-related factor 2 (Nrf2), wherein Nrf2 further mediated the expression of multiple antioxidant enzymes such as, heme oxygenase-1 (HO-1), NAD(P)H: quinone oxidoreductase-1 (NQO1) and catalase, which are closely related with redox homeostasis. DHA treatment also restored MSU-induced impairment of mitochondrial transmembrane potential. In addition, oral administration of DHA-rich microalgal oil to C57BL/6 mice effectively reduced the infiltration of neutrophils, and decreased the expression and secretion of inflammatory cytokines. Altogether, our results suggest that DHA or DHA-rich microalgal oil may be a promising natural agent for the prevention of MSU-induced inflammation and potentially acute gout at least partly by attenuating oxidative stress.
DHA and DHA-rich microalgal oil protect against monosodium urate-induced inflammation
via
regulating oxidative stress and inhibiting NLRP3-mediated inflammatory cytokine secretion.</description><identifier>ISSN: 2042-6496</identifier><identifier>EISSN: 2042-650X</identifier><identifier>DOI: 10.1039/c9fo00573k</identifier><identifier>PMID: 31214670</identifier><language>eng</language><publisher>England: Royal Society of Chemistry</publisher><subject>Animals ; Antioxidants ; Antioxidants - pharmacology ; Catalase ; Catalase - metabolism ; Cell Survival - drug effects ; Cytokines ; Cytokines - metabolism ; Docosahexaenoic acid ; Docosahexaenoic Acids - pharmacology ; Docosahexaenoic Acids - therapeutic use ; Gout ; Heme ; Heme oxygenase (decyclizing) ; Heme Oxygenase-1 - metabolism ; Homeostasis ; Homeostasis - drug effects ; Humans ; IL-1β ; Immune system ; Infiltration ; Inflammation ; Inflammation - chemically induced ; Inflammation - drug therapy ; Inflammation - immunology ; Interleukin-1beta - metabolism ; Interleukins ; Leukocytes (neutrophilic) ; Male ; Membrane potential ; Membrane Potential, Mitochondrial ; Metastases ; Mice ; Mice, Inbred C57BL ; Microalgae ; Mitochondria ; NAD ; NAD(P)H Dehydrogenase (Quinone) - metabolism ; Neutrophils - drug effects ; NF-E2-Related Factor 2 - metabolism ; Nuclear transport ; Oral administration ; Oxidative stress ; Oxidative Stress - drug effects ; Oxygenase ; Phagocytosis ; Protective Agents - pharmacology ; Quinone oxidoreductase ; Quinones ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; THP-1 Cells ; Translocation ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Uric acid ; Uric Acid - adverse effects</subject><ispartof>Food & function, 2019-07, Vol.1 (7), p.41-421</ispartof><rights>Copyright Royal Society of Chemistry 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c378t-ea1cbe608f2d34cbe5dc8893637192a9c84009e46dd206b4d31e489ad1bbb9b83</citedby><cites>FETCH-LOGICAL-c378t-ea1cbe608f2d34cbe5dc8893637192a9c84009e46dd206b4d31e489ad1bbb9b83</cites><orcidid>0000-0001-8056-0953</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31214670$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Yue</creatorcontrib><creatorcontrib>Liu, Lu</creatorcontrib><creatorcontrib>Sun, Dongzhe</creatorcontrib><creatorcontrib>He, Yongjing</creatorcontrib><creatorcontrib>Jiang, Yue</creatorcontrib><creatorcontrib>Cheng, Ka-Wing</creatorcontrib><creatorcontrib>Chen, Feng</creatorcontrib><title>DHA protects against monosodium urate-induced inflammation through modulation of oxidative stress</title><title>Food & function</title><addtitle>Food Funct</addtitle><description>Acute gouty inflammation could be triggered by phagocytosis of monosodium urate (MSU) by immune cells. This study investigated the protective effect and underlying mechanism of docosahexaenoic acid (DHA) on MSU-induced inflammation
in vitro
and
in vivo
. Results showed that DHA effectively inhibited MSU-induced expression and secretion of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in THP-1 cells. Intracellular reactive oxygen species (ROS) production triggered by MSU was alleviated by DHA treatment. Furthermore, DHA promoted the nuclear translocation of nuclear factor E2-related factor 2 (Nrf2), wherein Nrf2 further mediated the expression of multiple antioxidant enzymes such as, heme oxygenase-1 (HO-1), NAD(P)H: quinone oxidoreductase-1 (NQO1) and catalase, which are closely related with redox homeostasis. DHA treatment also restored MSU-induced impairment of mitochondrial transmembrane potential. In addition, oral administration of DHA-rich microalgal oil to C57BL/6 mice effectively reduced the infiltration of neutrophils, and decreased the expression and secretion of inflammatory cytokines. Altogether, our results suggest that DHA or DHA-rich microalgal oil may be a promising natural agent for the prevention of MSU-induced inflammation and potentially acute gout at least partly by attenuating oxidative stress.
DHA and DHA-rich microalgal oil protect against monosodium urate-induced inflammation
via
regulating oxidative stress and inhibiting NLRP3-mediated inflammatory cytokine secretion.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Catalase</subject><subject>Catalase - metabolism</subject><subject>Cell Survival - drug effects</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Docosahexaenoic acid</subject><subject>Docosahexaenoic Acids - pharmacology</subject><subject>Docosahexaenoic Acids - therapeutic use</subject><subject>Gout</subject><subject>Heme</subject><subject>Heme oxygenase (decyclizing)</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Homeostasis</subject><subject>Homeostasis - drug effects</subject><subject>Humans</subject><subject>IL-1β</subject><subject>Immune system</subject><subject>Infiltration</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - immunology</subject><subject>Interleukin-1beta - metabolism</subject><subject>Interleukins</subject><subject>Leukocytes (neutrophilic)</subject><subject>Male</subject><subject>Membrane potential</subject><subject>Membrane Potential, Mitochondrial</subject><subject>Metastases</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microalgae</subject><subject>Mitochondria</subject><subject>NAD</subject><subject>NAD(P)H Dehydrogenase (Quinone) - metabolism</subject><subject>Neutrophils - drug effects</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Nuclear transport</subject><subject>Oral administration</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxygenase</subject><subject>Phagocytosis</subject><subject>Protective Agents - pharmacology</subject><subject>Quinone oxidoreductase</subject><subject>Quinones</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>THP-1 Cells</subject><subject>Translocation</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Uric acid</subject><subject>Uric Acid - adverse effects</subject><issn>2042-6496</issn><issn>2042-650X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc9LwzAUx4MobsxdvCsFLyJUkyZtk-OYzomDXRS8lTRJt862mfkh-t-buR-C75L38j7vy8s3AJwjeIsgZneCVRrCNMfvR6CfQJLEWQrfjvc5YVkPDK1dwRCYMcroKehhlCCS5bAP-P10FK2Ndko4G_EFrzvrolZ32mpZ-zbyhjsV1530Qsmo7qqGty13te4itzTaL5aBlr7ZXukq0l-1DMWniqwzytozcFLxxqrh7hyA18nDy3gaz-aPT-PRLBY4py5WHIlSZZBWicQkpKkUlDKc4RyxhDNBCYRMkUzKBGYlkRgpQhmXqCxLVlI8ANdb3fCaD6-sK9raCtU0vFPa2yJJCA4DOcQBvfqHrrQ3XdguUCnNc5pmG8GbLSWMttaoqlibuuXmu0Cw2HhfjNlk_uv9c4Avd5K-bJU8oHunA3CxBYwVh-7f5-EfI3aJzw</recordid><startdate>20190717</startdate><enddate>20190717</enddate><creator>Zhang, Yue</creator><creator>Liu, Lu</creator><creator>Sun, Dongzhe</creator><creator>He, Yongjing</creator><creator>Jiang, Yue</creator><creator>Cheng, Ka-Wing</creator><creator>Chen, Feng</creator><general>Royal Society of Chemistry</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>7T5</scope><scope>7T7</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8056-0953</orcidid></search><sort><creationdate>20190717</creationdate><title>DHA protects against monosodium urate-induced inflammation through modulation of oxidative stress</title><author>Zhang, Yue ; Liu, Lu ; Sun, Dongzhe ; He, Yongjing ; Jiang, Yue ; Cheng, Ka-Wing ; Chen, Feng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c378t-ea1cbe608f2d34cbe5dc8893637192a9c84009e46dd206b4d31e489ad1bbb9b83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Catalase</topic><topic>Catalase - metabolism</topic><topic>Cell Survival - drug effects</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Docosahexaenoic acid</topic><topic>Docosahexaenoic Acids - pharmacology</topic><topic>Docosahexaenoic Acids - therapeutic use</topic><topic>Gout</topic><topic>Heme</topic><topic>Heme oxygenase (decyclizing)</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Homeostasis</topic><topic>Homeostasis - drug effects</topic><topic>Humans</topic><topic>IL-1β</topic><topic>Immune system</topic><topic>Infiltration</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - immunology</topic><topic>Interleukin-1beta - metabolism</topic><topic>Interleukins</topic><topic>Leukocytes (neutrophilic)</topic><topic>Male</topic><topic>Membrane potential</topic><topic>Membrane Potential, Mitochondrial</topic><topic>Metastases</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microalgae</topic><topic>Mitochondria</topic><topic>NAD</topic><topic>NAD(P)H Dehydrogenase (Quinone) - metabolism</topic><topic>Neutrophils - drug effects</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Nuclear transport</topic><topic>Oral administration</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxygenase</topic><topic>Phagocytosis</topic><topic>Protective Agents - pharmacology</topic><topic>Quinone oxidoreductase</topic><topic>Quinones</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>THP-1 Cells</topic><topic>Translocation</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Uric acid</topic><topic>Uric Acid - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Yue</creatorcontrib><creatorcontrib>Liu, Lu</creatorcontrib><creatorcontrib>Sun, Dongzhe</creatorcontrib><creatorcontrib>He, Yongjing</creatorcontrib><creatorcontrib>Jiang, Yue</creatorcontrib><creatorcontrib>Cheng, Ka-Wing</creatorcontrib><creatorcontrib>Chen, Feng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Food & function</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Yue</au><au>Liu, Lu</au><au>Sun, Dongzhe</au><au>He, Yongjing</au><au>Jiang, Yue</au><au>Cheng, Ka-Wing</au><au>Chen, Feng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DHA protects against monosodium urate-induced inflammation through modulation of oxidative stress</atitle><jtitle>Food & function</jtitle><addtitle>Food Funct</addtitle><date>2019-07-17</date><risdate>2019</risdate><volume>1</volume><issue>7</issue><spage>41</spage><epage>421</epage><pages>41-421</pages><issn>2042-6496</issn><eissn>2042-650X</eissn><abstract>Acute gouty inflammation could be triggered by phagocytosis of monosodium urate (MSU) by immune cells. This study investigated the protective effect and underlying mechanism of docosahexaenoic acid (DHA) on MSU-induced inflammation
in vitro
and
in vivo
. Results showed that DHA effectively inhibited MSU-induced expression and secretion of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in THP-1 cells. Intracellular reactive oxygen species (ROS) production triggered by MSU was alleviated by DHA treatment. Furthermore, DHA promoted the nuclear translocation of nuclear factor E2-related factor 2 (Nrf2), wherein Nrf2 further mediated the expression of multiple antioxidant enzymes such as, heme oxygenase-1 (HO-1), NAD(P)H: quinone oxidoreductase-1 (NQO1) and catalase, which are closely related with redox homeostasis. DHA treatment also restored MSU-induced impairment of mitochondrial transmembrane potential. In addition, oral administration of DHA-rich microalgal oil to C57BL/6 mice effectively reduced the infiltration of neutrophils, and decreased the expression and secretion of inflammatory cytokines. Altogether, our results suggest that DHA or DHA-rich microalgal oil may be a promising natural agent for the prevention of MSU-induced inflammation and potentially acute gout at least partly by attenuating oxidative stress.
DHA and DHA-rich microalgal oil protect against monosodium urate-induced inflammation
via
regulating oxidative stress and inhibiting NLRP3-mediated inflammatory cytokine secretion.</abstract><cop>England</cop><pub>Royal Society of Chemistry</pub><pmid>31214670</pmid><doi>10.1039/c9fo00573k</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-8056-0953</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2042-6496 |
| ispartof | Food & function, 2019-07, Vol.1 (7), p.41-421 |
| issn | 2042-6496 2042-650X |
| language | eng |
| recordid | cdi_crossref_primary_10_1039_C9FO00573K |
| source | MEDLINE; Royal Society Of Chemistry Journals 2008- |
| subjects | Animals Antioxidants Antioxidants - pharmacology Catalase Catalase - metabolism Cell Survival - drug effects Cytokines Cytokines - metabolism Docosahexaenoic acid Docosahexaenoic Acids - pharmacology Docosahexaenoic Acids - therapeutic use Gout Heme Heme oxygenase (decyclizing) Heme Oxygenase-1 - metabolism Homeostasis Homeostasis - drug effects Humans IL-1β Immune system Infiltration Inflammation Inflammation - chemically induced Inflammation - drug therapy Inflammation - immunology Interleukin-1beta - metabolism Interleukins Leukocytes (neutrophilic) Male Membrane potential Membrane Potential, Mitochondrial Metastases Mice Mice, Inbred C57BL Microalgae Mitochondria NAD NAD(P)H Dehydrogenase (Quinone) - metabolism Neutrophils - drug effects NF-E2-Related Factor 2 - metabolism Nuclear transport Oral administration Oxidative stress Oxidative Stress - drug effects Oxygenase Phagocytosis Protective Agents - pharmacology Quinone oxidoreductase Quinones Reactive oxygen species Reactive Oxygen Species - metabolism THP-1 Cells Translocation Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α Uric acid Uric Acid - adverse effects |
| title | DHA protects against monosodium urate-induced inflammation through modulation of oxidative stress |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T13%3A20%3A54IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=DHA%20protects%20against%20monosodium%20urate-induced%20inflammation%20through%20modulation%20of%20oxidative%20stress&rft.jtitle=Food%20&%20function&rft.au=Zhang,%20Yue&rft.date=2019-07-17&rft.volume=1&rft.issue=7&rft.spage=41&rft.epage=421&rft.pages=41-421&rft.issn=2042-6496&rft.eissn=2042-650X&rft_id=info:doi/10.1039/c9fo00573k&rft_dat=%3Cproquest_cross%3E2243489703%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2258778568&rft_id=info:pmid/31214670&rfr_iscdi=true |