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In diseased rats, selective COX-2 inhibition resulted in 18% and 67% reduction in cystic expansion and interstitial fibrosis, respectively, but no change in renal function. NS-398 also ameliorated disease-associated pathologies, such as renal inflammation, cell proliferation, and oxidant injury (by 33, 38, and 59%, respectively). Kidney disease was associated with elevated renal COX-1 and COX-2 enzyme activities, and NS-398 blunted the increase in COX-2 enzyme activity (as indicated by 21 and 28% lower renal thromboxane B<jats:sub>2<\/jats:sub>and PGE<jats:sub>2<\/jats:sub>levels, respectively). NS-398 reduced urinary excretion of prostanoid metabolites in diseased rats. In summary, COX-2 inhibition attenuated renal injury, reduced the elevated renal COX-2 activity, and ameliorated disease-related alterations in prostanoid production in this rat model of chronic renal disease.<\/jats:p>","DOI":"10.1152\/ajprenal.00257.2006","type":"journal-article","created":{"date-parts":[[2007,5,31]],"date-time":"2007-05-31T01:04:40Z","timestamp":1180573480000},"page":"F821-F830","source":"Crossref","is-referenced-by-count":61,"title":["Selective COX-2 inhibition markedly slows disease progression and attenuates altered prostanoid production in Han:SPRD-<i>cy<\/i>rats with inherited kidney disease"],"prefix":"10.1152","volume":"293","author":[{"given":"Deepa","family":"Sankaran","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Neda","family":"Bankovic-Calic","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Malcolm 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