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Am J Physiol Renal Physiol (February 14, 2006). doi:10.1152/ajprenal.00412.2005
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Submitted on October 19, 2005
Accepted on February 7, 2006

Anti-inflammatory and anti-necrotic effects of the volatile anesthetic sevoflurane in kidney proximal tubule cells

H. Thomas Lee1*, Mihwa Kim1, Michael Jan1, and Charles W Emala1

1 Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, NY, USA

* To whom correspondence should be addressed. E-mail: tl128{at}columbia.edu.

Renal ischemia reperfusion (IR) injury is a major clinical problem without effective therapy. We recently reported that volatile anesthetics protect against renal IR injury in part via their anti-inflammatory properties. In this study, we demonstrate the anti-inflammatory and anti-necrotic effects of sevoflurane in cultured kidney proximal tubule cells and probed the mechanisms of sevoflurane-induced renal cellular protection. To mimic inflammation, human kidney proximal tubule (HK-2) cells were treated with tumor necrosis factor-alpha (TNF-{alpha}, 25 ng/ml) in the presence or absence of sevoflurane. In addition, we studied the effects of sevoflurane pretreatment on hydrogen peroxide (H2O2)-induced necrotic cell death in HK-2 or porcine proximal tubule (LLC-PK1) cells. We demonstrate that sevoflurane suppressed pro-inflammatory effects of TNF- {alpha} evidenced by attenuated up-regulation of pro-inflammatory cytokine mRNA (TNF-{alpha}, MCP-1) and ICAM-1 protein and reduced nuclear translocation of the pro-inflammatory transcription factors NF-{kappa}B and AP-1. Sevoflurane reduced necrotic cell death induced with H2O2 in HK-2 cells as well as in LLC-PK1 cells. Sevoflurane treatment resulted in phosphorylation of pro-survival kinases, ERK and Akt, and increased de novo HSP70 protein synthesis without affecting the synthesis of HSP27 or HSP32. We conclude that sevoflurane has direct anti-inflammatory and anti-necrotic effects in vitro in a renal cell type particularly sensitive to injury following IR injury. These mechanisms may in part account for volatile anesthetics' protective effects against renal IR injury.




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