OBJECTIVES: Ischemia/reperfusion (I/R) injury in the kidney during perioperative period remains the leading cause of acute renal failure. The purpose of this experimental study was to determine the role of dexmedetomidine (Dex) on renal I/R injury in rats. MATERIALS AND METHODS: Male Wistar rats, subjected to renal ischemia for 45 min, were either untreated or treated with dexmedetomidine 30 min prior to renal ischemia. A sham-operated group served as the control. Renal function [serum creatinine, blood urea nitrogen, serum Cystatin C and neutrophil gelatinase-associated lipocalin (NGAL)], histology, apoptosis and expression of the phosphorylations of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) were assessed. RESULTS: The animals treated with dexmedetomidine improved renal functional recovery, especially reducing the level of serum Cystatin C and NGAL at early time after ischemia, attenuated histological lesions, reduced tubular epithelial apoptosis and inhibited the phosphorylation of JAK2 and its downstream molecule STAT3, contributing to ameliorating renal I/R injury. CONCLUSIONS: Our data suggest that anti-apoptosis effect contributes to the renoprotection of dexmedetomidine, via inhibiting JAK2/STAT3 signaling pathway partially.
OBJECTIVES:Ischemia/reperfusion (I/R) injury in the kidney during perioperative period remains the leading cause of acute renal failure. The purpose of this experimental study was to determine the role of dexmedetomidine (Dex) on renal I/R injury in rats. MATERIALS AND METHODS: Male Wistar rats, subjected to renal ischemia for 45 min, were either untreated or treated with dexmedetomidine 30 min prior to renal ischemia. A sham-operated group served as the control. Renal function [serum creatinine, blood ureanitrogen, serum Cystatin C and neutrophil gelatinase-associated lipocalin (NGAL)], histology, apoptosis and expression of the phosphorylations of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) were assessed. RESULTS: The animals treated with dexmedetomidine improved renal functional recovery, especially reducing the level of serum Cystatin C and NGAL at early time after ischemia, attenuated histological lesions, reduced tubular epithelial apoptosis and inhibited the phosphorylation of JAK2 and its downstream molecule STAT3, contributing to ameliorating renal I/R injury. CONCLUSIONS: Our data suggest that anti-apoptosis effect contributes to the renoprotection of dexmedetomidine, via inhibiting JAK2/STAT3 signaling pathway partially.
Authors: Flavia Ps Freitas; Marcella L Porto; Camilla P Tranhago; Rogerio Piontkowski; Emilio C Miguel; Thaiz Bar Miguel; Jorge L Martins; Kyria S Nascimento; Camille M Balarini; Benildo S Cavada; Silvana S Meyrelles; Elisardo C Vasquez; Agata L Gava Journal: Am J Transl Res Date: 2015-12-15 Impact factor: 4.060