Renal
ischemia-reperfusion (I/R) injury is a major cause of
acute kidney injury via
inflammation and cell apoptosis. Volatile
anesthetics have been shown to exert organ-protective effects against kidney damage in vivo and in vitro. In the present study, we investigated the effects of
isoflurane, a commonly used volatile
anesthetic, on renal I/R injury and the underlying mechanisms. Rats subjected to renal I/R displayed higher serum
creatinine and blood
urea nitrogen levels than
sham rats as well as severe histopathological damage. Renal I/R also resulted in a nuclear factor-κB (NF-κB)-mediated inflammatory response and dysfunction of the p53-Bax-caspase-3 apoptotic pathway. Rats preconditioned with 1.5%
isoflurane for 2 h had better renal function and less tubular apoptosis 24 h after I/R injury than control rats. Pretreatment with
isoflurane suppressed renal NF-κB activation, leading to a reduction in proinflammatory molecules (high-mobility group box 1,
interleukin-1β, and
tumor necrosis factor-α) both in the kidneys and circulation. In addition, rats subjected to
isoflurane preconditioning had a higher Bcl-2/Bax ratio and less cleaved
caspase-3. Our findings suggest that preconditioning with a clinically relevant concentration of
isoflurane attenuates renal I/R injury, based at least in part on its ability to modulate renal
inflammation and apoptosis.