HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 295/4/F942    most recent 90236.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Liu, H. Articles by Yang, T. Search for Related Content PubMed PubMed Citation Articles by Liu, H. Articles by Yang, T.

Nitro-oleic acid protects the mouse kidney from ischemia and reperfusion injury

¹Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City; ²Department of Nephrology, 2nd Affiliated Hospital, Shandong University, Jinan, China; Departments of ³Physiology and ⁴Cellular Biology and Anatomy, Medical College of Georgia, and ⁵Medical Research Service, Veterans Affairs Medical Center, Augusta, Georgia; and ⁶College of Health University of Utah, Salt Lake City, Utah

Submitted 3 April 2008 ; accepted in final form 9 June 2008

Nitroalkene derivatives of linoleic acid (nitrolinoleic acid; LNO₂) and nitro-oleic acid (OA-NO₂) are endogenous lipid products with potent anti-inflammatory properties. The present study was undertaken to evaluate the therapeutic potential of OA-NO₂ in a mouse model of renal ischemia-reperfusion (I/R) injury. B6129SF2/J mice were subjected to bilateral renal ischemia for 30 min, followed by 24 h of reperfusion. Fifty minutes after ischemia, mice received intraperitoneal (ip) injections of OA-NO₂ (500 µg/kg; I/R OA-NO₂), vehicle for OA-NO₂ (i.e., 0.8 ml/kg ethanol; I/R veh), or oleic acid (500 µg/kg; I/R OA) every 6 h during the 24-h recovery period. A sham-operated group was not subjected to ischemia and received 0.8 ml/kg ethanol ip every 6 h during the 24-h recovery period (sham veh). While plasma urea and creatinine were elevated (P < 0.05) in I/R veh vs. sham veh mice, the severity was less (P < 0.05) in I/R OA-NO₂ animals. Indices of histological damage, polymorphonucleocyte infiltration, together with expression of intracellular adhesion molecule-1, interleukin-1β, and tumor necrosis factor-, p47^phox, and gp91^phox were greater in I/R veh vs. sham veh mice, but were attenuated (P < 0.05) in I/R OA-NO₂ animals. Because indices of renal dysfunction were similar between I/R veh and I/R OA mice (P > 0.05), but less (P < 0.05) in I/R OA-NO₂ animals compared with both groups, protection from bilateral renal ischemia is afforded by the nitrated but not free form of oleic acid. Together, delayed administration of nitrated fatty acid OA-NO₂ attenuates renal I/R injury in the mouse likely via inhibition of the inflammatory response.

nitrated fatty acids; acute renal failure; inflammation