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Am J Physiol Renal Physiol (May 30, 2007). doi:10.1152/ajprenal.00257.2006
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Submitted on July 6, 2006
Accepted on May 25, 2007

Selective COX-2 inhibition markedly slows disease progression and attenuates altered prostanoid production in Han:SPRD-cy rats with inherited kidney disease

Deepa Sankaran1, Neda Bankovic-Calic2, Malcolm R Ogborn3, Gary Crow4, and Harold M. Aukema5*

1 Human Nutritional Sciences, University of Manitoba, Winnipeg, Canada
2 Pediatrics and Child Health, University of Manitoba, Winnipeg, Canada
3 Human Nutritional Sciences, University of Manitoba, Winnipeg, Canada; Manitoba Institute of Child Health, Winnipeg, Canada; Pediatrics and Child Health, University of Manitoba, Winnipeg, Canada
4 Animal Sciences, University of Manitoba, Winnipeg, Canada
5 Human Nutritional Sciences, University of Manitoba, Winnipeg, Canada; Manitoba Institute of Child Health, Winnipeg, Canada

* To whom correspondence should be addressed. E-mail: aukemahm{at}cc.umanitoba.ca.

Selective cyclooxygenase -2 (COX-2) inhibitors appear to have beneficial reno-protective effects in most, but not all, renal disease conditions. The objective of our study was to examine the effects of COX-2 inhibition in a rat model of polycystic kidney disease. Four week old Han:SPRD-cy rats were given either a standard rodent diet containing 3mg NS398 kg body weight-1 day-1 or a control diet with no drug for 7 weeks. In diseased rats, selective COX-2 inhibition resulted in an 18% and 67% reduction in cystic expansion and interstitial fibrosis respectively without altering renal function. Disease-associated pathologies such as renal inflammation, cell proliferation, and oxidant injury also were ameliorated (by 33, 38 and 59% respectively) with NS398 treatment. Kidney disease was associated with elevated renal COX-1 and -2 enzyme activities and treatment with NS398 blunted the increase in COX-2 enzyme activity (as indicated by 21% and 28% lower renal thromboxane B2 and prostaglandin E2 levels, respectively). Urinary excretion of prostanoid metabolites in diseased rats was further reduced with NS398. 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.




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