Abstract
Objective To investigate the effect of dexmedetomidine on inflammation induced by renal ischemia and reperfusion injury (IRI) in rats.Methods Twenty SD rats were randomly divided into three groups:sham operated group,IRI group and dexmedetomidine group.Each group had 8 rats.In sham operated group,the right kidneys of rats were excised.In IRI group,with no wound vascular clamp,left renal arteries and veins of rats were clamped for 45 min,then vascular clamp was opened and the rats were subjected to repeffusion.In Dexmedetomidine groups,operation steps were the same as the IRI group,but at 30 min before ischemia,dexmedetomidine was given by intraperitoneal injection (100 μg/kg).The parameters [blood urea nitrogen (BUN) and ereatine (Cr)] for renal function were determined by auto-biochemieal analyzer.The expression levels of tumor necrosis factor (TNF)-α,interleukin (IL)-1 β and intercellular adhesion molecule-1 (ICAM-1) were measured by real-time fluorescent quantitative polymerase chain reaction (FQ-PCR) and the changes of renal tissue were examined by a microscope.The expression of Toll-like receptor4 (TLR4) and nuclear factor-κB (NF-κB) was detected by Western blotting.Results In sham group,IRI group and dexmedetomidine group,Cr levels (μmol/L) were 17.55 ± 1.02,138.49 ± 6.20 and 81.98 ±4.24,respectively,and BUN levels (mmol/L) were 7.00 ±2.06,27.38 ±4.37 and 13.75 ±3.54,respectively.Cr and BUN levels in sham operated group were obviously lower than in IRI group and dexmedetomidine group,and those in IRI group were significantly higher than in dexmedetomidine group.As compared with sham operated group,TNF-α,IL-1β,ICAM-1,TLR4 and NF-κB were significantly increased in IRI group and dexmedetomidine group.However,these targets in dexmedetomidine group were significantly decreased as compared with those in IRI group.Conclusion Dexmedetomidine can alleviate inflammation induced by renal IRI probably by inhibiting the expression of TLR4/NF-κB signaling pathway. Key words: Dexmedetomidine ; Renal schemia ; Reperfusion injury; Toll-like receptor 4 ; Nuclear factor-κB
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