{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T05:43:05Z","timestamp":1777873385866,"version":"3.51.4"},"reference-count":42,"publisher":"Frontiers Media SA","issue":"7","license":[{"start":{"date-parts":[[2009,7,1]],"date-time":"2009-07-01T00:00:00Z","timestamp":1246406400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Exp Biol Med (Maywood)"],"published-print":{"date-parts":[[2009,7]]},"abstract":"<jats:p>\n                    Increasing evidence in human chronic kidney disease and in animal models indicates the potential utility of dietary soy protein in the treatment of this disorder. A model in which a beneficial soy protein effect has been consistently demonstrated is the Han:SPRD- cy rat model of polycystic kidney disease. Therefore, since dietary soy protein alters renal hemodynamics and prostanoid production, the effects of dietary soy protein on renal prostanoids and related rate-limiting enzymes were examined. Normal and diseased weanling rats were given diets containing casein or soy protein for 7 wk. At 10 wk of age, renal levels of thromboxane B\n                    <jats:sub>2<\/jats:sub>\n                    (TXB\n                    <jats:sub>2<\/jats:sub>\n                    , stable metabolite of TXA\n                    <jats:sub>2<\/jats:sub>\n                    ), prostaglandin E\n                    <jats:sub>2<\/jats:sub>\n                    (PGE\n                    <jats:sub>2<\/jats:sub>\n                    ) and 6-keto PGF\n                    <jats:sub>1\u03b1<\/jats:sub>\n                    (stable metabolite of PGI\n                    <jats:sub>2<\/jats:sub>\n                    ) and activities of cyclooxygenase 1 (COX1) and COX2 were elevated in diseased compared to normal kidneys. Soy protein feeding resulted in 49% lower in vitro steady-state levels of TXB\n                    <jats:sub>2<\/jats:sub>\n                    , and 76% less 6-keto PGF\n                    <jats:sub>1\u03b1<\/jats:sub>\n                    produced by COX1 activity in diseased kidneys, while not altering these parameters in normal kidneys. It also resulted in 47% less TXB\n                    <jats:sub>2<\/jats:sub>\n                    and 36% lower 6-keto PGF\n                    <jats:sub>1\u03b1<\/jats:sub>\n                    produced by COX2 activity in diseased kidneys. The relative effect of soy protein feeding on COX2 activity was in the order of TXB\n                    <jats:sub>2<\/jats:sub>\n                    &gt; 6-keto PGF\n                    <jats:sub>1\u03b1<\/jats:sub>\n                    &gt; PGE\n                    <jats:sub>2<\/jats:sub>\n                    . Diseased kidneys had elevated protein and mRNA levels of cytosolic phospholipase A\n                    <jats:sub>2<\/jats:sub>\n                    (cPLA\n                    <jats:sub>2<\/jats:sub>\n                    ) and COX1 and lower levels of COX2. Dietary soy protein attenuated the protein levels of cPLA\n                    <jats:sub>2<\/jats:sub>\n                    in diseased kidneys, and reduced COX2 mRNA expression in both normal and diseased kidneys. Dietary soy protein therefore reduced the levels of specific renal prostanoids, cPLA\n                    <jats:sub>2<\/jats:sub>\n                    and COX enzymes in this model of polycystic kidney disease, a model in which soy protein has been demonstrated to reduce disease progression.\n                  <\/jats:p>","DOI":"10.3181\/0811-rm-315","type":"journal-article","created":{"date-parts":[[2009,5,8]],"date-time":"2009-05-08T22:00:08Z","timestamp":1241820008000},"page":"737-743","source":"Crossref","is-referenced-by-count":21,"title":["Dietary Soy Protein Selectively Reduces Renal Prostanoids and Cyclooxygenases in Polycystic Kidney Disease"],"prefix":"10.3389","volume":"234","author":[{"given":"Claudia Yu-Chen","family":"Peng","sequence":"first","affiliation":[{"name":"Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2; Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba, Canada R3A 1S1; and Manitoba Institute of Child Health, Winnipeg, Manitoba, Canada R3E 3P4"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Deepa","family":"Sankaran","sequence":"additional","affiliation":[{"name":"Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2; Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba, Canada R3A 1S1; and Manitoba Institute of Child Health, Winnipeg, Manitoba, Canada R3E 3P4"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Malcolm R.","family":"Ogborn","sequence":"additional","affiliation":[{"name":"Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2; Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba, Canada R3A 1S1; and Manitoba Institute of Child Health, Winnipeg, Manitoba, Canada R3E 3P4"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Harold M.","family":"Aukema","sequence":"additional","affiliation":[{"name":"Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2; Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba, Canada R3A 1S1; and Manitoba Institute of Child Health, Winnipeg, Manitoba, Canada R3E 3P4"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2009,7,1]]},"reference":[{"key":"bibr-R1","doi-asserted-by":"publisher","DOI":"10.1042\/CS20050251"},{"key":"bibr-R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00454.2004"},{"key":"bibr-R3","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.70.113006.100614"},{"key":"bibr-R4","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4684-5700-1_11"},{"key":"bibr-R5","doi-asserted-by":"publisher","DOI":"10.1016\/S1098-8823(03)00075-3"},{"key":"bibr-R7","doi-asserted-by":"publisher","DOI":"10.2337\/dc07-2065"},{"key":"bibr-R8","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ejcn.1601688"},{"key":"bibr-R9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V102300"},{"key":"bibr-R10","doi-asserted-by":"publisher","DOI":"10.1016\/j.jnutbio.2007.03.001"},{"key":"bibr-R11","doi-asserted-by":"crossref","unstructured":"Ogborn MR, Bankovic-Calic N, Shoesmith C, Buist R, Peeling J. 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