• Satoshi Hagiwara, Hironori Koga, Hideo Iwasaka, Kyosuke Kudo, Akira Hasegawa, Jyunya Kusaka, Isao Yokoi, and Takayuki Noguchi.
• Department of Anesthesiology and Intensive Care Medicine, Oita University Faculty of Medicine, Oita, Japan. saku@med.oita-u.ac.jp
• J. Surg. Res. 2011 Nov 1; 171 (1): 226-33.

BackgroundIschemia-reperfusion (I/R) contributes to acute kidney injury (AKI). On the other hand, anti-oxidative drugs help to prevent renal injury caused by I/R. The current study examined whether a new antioxidant, ETS-GS, inhibits reactive oxygen species (ROS) generation and thereby prevents renal I/R injury in rodent models.MethodsRats with experimentally-induced renal I/R injury were treated concurrently with an intravenous injection of either ETS-GS or saline. Anesthesia was induced with sevoflurane.ResultsHistologic examination revealed marked reduction of interstitial congestion, edema, inflammation, and hemorrhage in kidney tissue harvested 24 h after ETS-GS treatment. Renal I/R-induced secretion of nitric oxide (NO) in serum was inhibited by ETS-GS treatment. Furthermore, malondialdehyde (MDA) levels in the kidney were significantly lower in ETS-GS-treated rats with renal I/R. Moreover, when murine macrophage-like RAW264.7 cells were stimulated with antimycin A in the presence or absence of simultaneous ETS-GS treatment, ETS-GS decreased ROS levels.ConclusionsThus, ETS-GS lowered ROS levels in cultured cells, reduced serum NO levels, decreased renal MDA levels, and protected rats against I/R-induced kidney injury. Given these in vitro and in vivo findings, ETS-GS is a strong candidate for future exploration of therapeutic potential in various human I/R diseases.Copyright © 2011 Elsevier Inc. All rights reserved.

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