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

Haiying Liu, Zhunjun Jia, Sunhapas Soodvilai, Guangju Guan, Mong-Heng Wang, Zheng Dong, J. David Symons, Tianxin Yang

Research output: Contribution to journalArticle

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Abstract

Nitroalkene derivatives of linoleic acid (nitrolinoleic acid; LNO 2) 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-α, p47phox, and gp91phox 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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Physiology
Volume295
Issue number4
DOIs
StatePublished - Jan 1 2008

Fingerprint

Oleic Acid
Reperfusion Injury
Ischemia
Kidney
Reperfusion
Ethanol
Linoleic Acid
Intraperitoneal Injections
Urea
Creatinine
Anti-Inflammatory Agents
Fatty Acids
Lipids

Keywords

  • Acute renal failure
  • Inflammation
  • Nitrated fatty acids

ASJC Scopus subject areas

  • Physiology
  • Urology

Cite this

Nitro-oleic acid protects the mouse kidney from ischemia and reperfusion injury. / Liu, Haiying; Jia, Zhunjun; Soodvilai, Sunhapas; Guan, Guangju; Wang, Mong-Heng; Dong, Zheng; Symons, J. David; Yang, Tianxin.

In: American Journal of Physiology - Renal Physiology, Vol. 295, No. 4, 01.01.2008.

Research output: Contribution to journalArticle

Liu, Haiying ; Jia, Zhunjun ; Soodvilai, Sunhapas ; Guan, Guangju ; Wang, Mong-Heng ; Dong, Zheng ; Symons, J. David ; Yang, Tianxin. / Nitro-oleic acid protects the mouse kidney from ischemia and reperfusion injury. In: American Journal of Physiology - Renal Physiology. 2008 ; Vol. 295, No. 4.
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AU - Wang, Mong-Heng

AU - Dong, Zheng

AU - Symons, J. David

AU - Yang, Tianxin

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AB - Nitroalkene derivatives of linoleic acid (nitrolinoleic acid; LNO 2) 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-α, p47phox, and gp91phox 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.

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