{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T07:53:20Z","timestamp":1791618800306,"version":"4.3.4"},"reference-count":56,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2017,10,13]],"date-time":"2017-10-13T00:00:00Z","timestamp":1507852800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Boehringer Ingelheim Animal Health GmbH, Ingelheim am Rhein, Germany"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Animal Physiology Nutrition"],"published-print":{"date-parts":[[2018,4]]},"abstract":"Summary<\/jats:title>Although it is well recognized that dietary supplementation with fish oil improves clinical symptoms in dogs suffering from osteoarthritis, the molecular basis for the dietary benefit is not yet completely resolved in dogs. This study was designed to further clarify how polyunsaturated fatty acids (PUFA<\/jats:styled-content>) affect key factors of cartilage degeneration in a canine cell culture system mimicking osteoarthritis. Canine chondrocytes were incubated either without or with 10\u00a0\u03bcm<\/jats:sc> of eicosapentaenoic acid (EPA<\/jats:styled-content>), docosahexaenoic acid (DHA<\/jats:styled-content>), arachidonic acid (AA<\/jats:styled-content>) or 3.6\u00a0\u03bcm<\/jats:sc> ibuprofen (Ibu) as positive control for 6\u00a0days. After the supplementation, cells were stimulated with 10\u00a0ng\/ml interleukin\u20101\u03b2 (IL<\/jats:styled-content>\u20101\u03b2) for another 48\u00a0hr to induce osteoarthritic changes, or left unstimulated. We analysed fatty acid uptake via gas\u2013liquid chromatography, nitric oxide (NO<\/jats:styled-content>) production via Griess assay, prostaglandin E (PGE<\/jats:styled-content>) production via ELISA<\/jats:styled-content> and relative gene expression of several cartilage matrix proteinases, inducible nitric oxide synthase (iNOS<\/jats:styled-content>) and cyclooxygenase\u20102 via RT<\/jats:styled-content>\u2010qPCR<\/jats:styled-content>. After supplementation, the chondrocytes rapidly incorporated the PUFA<\/jats:styled-content> into their fatty acid pools. The stimulation with IL<\/jats:styled-content>\u20101\u03b2 caused a marked increase of most of the inflammatory markers measured. N\u20103 PUFA EPA<\/jats:styled-content> reduced IL<\/jats:styled-content>\u2010induced gene expression of iNOS<\/jats:styled-content> and corresponding production of NO<\/jats:styled-content>. N\u20106 PUFA AA<\/jats:styled-content> also decreased iNOS<\/jats:styled-content> and NO<\/jats:styled-content>, but furthermore lowered gene expression of matrix metalloproteinase\u20103. On the other hand, AA<\/jats:styled-content> upregulated the aggrecanase ADAMTS<\/jats:styled-content>\u20105 and augmented the release of PGE<\/jats:styled-content>. The effect of n\u20103 PUFA DHA<\/jats:styled-content> turned out to be negligible. Our results reveal molecular mechanisms by which PUFA<\/jats:styled-content> affect degenerative joint disease in dogs. Of particular importance is that not only EPA<\/jats:styled-content> but also AA<\/jats:styled-content> decreased several inflammatory markers in our model. Thus, we conclude that an appropriate balance of both n\u20103 and n\u20106 fatty acids deserves more attention in dietary interventions.<\/jats:p>","DOI":"10.1111\/jpn.12804","type":"journal-article","created":{"date-parts":[[2017,10,14]],"date-time":"2017-10-14T04:22:47Z","timestamp":1507954967000},"source":"Crossref","is-referenced-by-count":37,"title":["Polyunsaturated fatty acids influence inflammatory markers in a cellular model for canine osteoarthritis"],"prefix":"10.1111","volume":"102","author":[{"given":"N.","family":"Adler","sequence":"first","affiliation":[{"name":"Institute of Biochemistry Faculty of Veterinary Medicine University of Leipzig Leipzig Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Schoeniger","sequence":"additional","affiliation":[{"name":"Institute of Biochemistry Faculty of Veterinary Medicine University of Leipzig Leipzig Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6767-4435","authenticated-orcid":false,"given":"H.","family":"Fuhrmann","sequence":"additional","affiliation":[{"name":"Institute of Biochemistry Faculty of Veterinary Medicine University of Leipzig Leipzig Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,10,13]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1063-4584(08)60008-4"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119280"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.abb.2006.09.014"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1093\/ajcn\/83.6.1467S"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.181.7.5082"},{"key":"e_1_2_6_7_1","first-page":"99","article-title":"Activation of diverse eicosanoid pathways in osteoarthritic cartilage. 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