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Am J Physiol Renal Physiol 294: F272-F280, 2008. First published November 21, 2007; doi:10.1152/ajprenal.00352.2007
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Effects of {alpha}-lipoic acid on ischemia-reperfusion-induced renal dysfunction in rats

Eun Hui Bae,1 Kyun Sang Lee,1 JongUn Lee,2 Seong Kwon Ma,1 Nam Ho Kim,1 Ki Chul Choi,1 Jørgen Frøkiær,4 Søren Nielsen,4 Sun Young Kim,5 Sung Zoo Kim,5 Suhn Hee Kim,5 and Soo Wan Kim1,3

Departments of 1Internal Medicine and 2Physiology and 3Cardiovascular Research Institute, Chonnam National University, Gwangju; 4The Water and Salt Research Center, University of Aarhus, Aarhus C, Denmark; and 5Department of Physiology, Chonbuk National University Medical School, Jeonju, Korea

Submitted 28 July 2007 ; accepted in final form 12 November 2007

We investigated whether {alpha}-lipoic acid ({alpha}-LA), an antioxidant, attenuates the ischemia-reperfusion (I/R)-induced dysregulation of these transporters. Both renal pedicles of male Sprague-Dawley rats were clamped for 40 min. {alpha}-LA (80 mg/kg) was administered intraperitoneally before and immediately after induction of ischemia. After 2 days, the expression of aquaporins (AQPs), sodium transporters, and nitric oxide synthases (NOS) was determined in the kidney by immunoblotting and immunohistochemistry. The expression of endothelin-1 (ET-1) mRNA was determined by real-time PCR. Activities of adenylyl cyclase and guanylyl cyclase were measured by stimulated generation of cAMP and cGMP, respectively. The expression of AQP1–3 as well as that of the {alpha}1-subunit of Na-K-ATPase, type 3 Na/H exchanger, Na-K-2Cl cotransporter, and Na-Cl cotransporter was markedly decreased in response to I/R. The expression of type VI adenylyl cyclase was decreased in I/R-injured rats, which was counteracted by the treatment of {alpha}-LA. AVP-stimulated cAMP generation was blunted in I/R rats and was then ameliorated by {alpha}-LA treatment. {alpha}-LA treatment attenuated the downregulation of AQPs and sodium transporters. The expression of endothelial NOS was decreased in I/R rats, which was prevented by {alpha}-LA. The cGMP generation in response to sodium nitroprusside was blunted in I/R rats, which was also significantly prevented by {alpha}-LA. The mRNA expression of ET-1 was increased, which was recovered to the control level by {alpha}-LA treatment. In conclusion, {alpha}-LA treatment prevents I/R-induced dysregulation of AQPs and sodium transporters in the kidney, possibly through preserving normal activities of local AVP/cAMP, nitric oxide/cGMP, and ET systems.

I/R injury; aquaporins; sodium transporters; nitric oxide; endothelin


Address for reprint requests and other correspondence: S. W. Kim, Dept. of Internal Medicine, Chonnam National Univ. Medical School, Hakdong 8, Gwangju 501-757, Korea (e-mail: skimw{at}chonnam.ac.kr)






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