Induction of stress response proteins and experimental renal ischemia/reperfusion

Background. The induction of stress response (heat shock) proteins (HSPs) i s a highly conserved response that protects many cell types fi om diverse p hysiological and environmental stressors. Si-e rested the hypothesis that t he induction of HSPs is protective in experimental renal ischemia/reperfusi on injury. Methods. The effect of prior heat stress was examined in a rat model of ren al ischemia. Postischemic renal function, histopathology, myeloperoxidase a ctivity, and mortality were determined in hyperthermia and sham hyperthermi a groups. Results. HSP84, HSP70, and HSP22 mRNA were increased after eight minutes bu t not four minutes of hyperthermia. The induction of HSP84 and HSP70 was bl ocked by pretreatment with quercetin, improvement in renal function, mortal ity, and histologic abnormalities was seen with eight minutes of hypertherm ia six hours before ischemia, Protection was dependent on the timing of isc hemia relative to heat stress and was not observed when HSPs were not induc ed. Postischemic increases in renal myeloperoxidase activity were markedly attenuated in the hyperthermia compared with the sham hyperthermia group. Conclusion. Endogenous protective mechanisms mag; be important in renal isc hemia/reperfusion injury.