Renoprotective effects and mechanism of dexmedetomidine on renal ischemia/reperfusion injury in rats

Objective To observe the effects of dexmedetomidine (DEX) on renal cell apoptosis and inflammatory factors against renal ischemia/reperfusion injury (IRI) in rats and investigate its mechanism.Methods Forty healthy male Wistar rats, weighing 220-300 g, were randomly allocated into 4 groups: control group(group C), ischemia/reperfusion group (group IR), atipamezole combined with dexmedetomidine group (group AD) and dexmedetomidine group (group DEX). We established the IRI model via clamping both renal pedicles of rats for 45 min with non-traumatic vascular clamps. Rats in control group underwent sham surgery only. Rats in the groups AD and DEX received dexmedetomidine 25 μg/kg via intraperitoneal injection 30 min before renal ischemia. Rats in the groups C and IR receive the same volume of saline only. Rats in the group AD were treated with atipamezole (250 μg/kg) prior to the administration of dexmedetomidine. At 24 h after reperfusion, renal tissue was obtained to observe histopathological changes and apoptosis, and to detect the expression of JAK2, STAT3, p-JAK2 and p-STAT3. The blood sample was obtained to detect the level of TNF-α, IL-6 and IL-10.Results Compared with groups IR and AD, there were less histopathological changes, less numbers of apoptosis cells, less expression of JAK2, STAT3, p-JAK2, p-STAT3, TNF-α, IL-6, and higher expression of IL-10 in group DEX (P0.05).Conclusion The administration of dexmedetomidine against renal IRI may regulate inflammatory factors via suppressing JAK2/STAT3 pathway, attenuate the renal inflammatory responses, suppress apoptosis, and lessen the injury of renal tissue.