Effects Of Dexmedetomidine On The Protection Of Sepsis-Induced Acute Kidney Injury And The Expression Of Hmgb1Mrna In Renal Tissues Of Septic Rats

ObjectiveTo observethe effects of dexmedetomidine (DEX) on the protection ofsepsis-induced acute kidney injury and the expression of HMGB1mRNA in renaltissues andthe level of serum cystatin C (Cys C)of septic rats, and to investigate thepotential mechanisms, then to introduce some novel strategies on sepsis in medicalpractice.Methods48healthymale SD rats, weighted240-270g, were assigned to3groups(n=16each) by random number table: sham operation group (SHAM group), modelgroup (CLP group), and dexmedetomidine group (DEX group). The rats in group CLPand DEX had cecal ligation and puncture (CLP) surgery to establish model of sepsis-induced acute kidney injury(AKI). Each rat in group DEX received intraperitonealinjection with40μg/kg of DEX at l hour after the surgery, while SHAM andCLPgroup received equal volume of normal saline instead. After harvestedbloodsamples,8of the rats in each group were randomly sacrificed respectively at24h,48hafter the surgery, and then kidney tissues were reserved. The levels of serum Cys Cwere measured by immunoturbidimetric assays, the expression of HMGB1mRNA inrenal tissueswas measured by real-time fluorescence quantitative PCR, andhistopathological examinations on renal tissues were observed under lightmicroscope.ResultsCompared with SHAMgroupat each time point,levels of the expressionof HMGB1mRNA in renal tissues and serum Cys C were significantly increased(P<0.05) in CLP and DEXgroup at24h and48h, respectively, and renal tissues hadhistopathological damages in various degrees. Compared with CLPgroup, levels ofthe expression of HMGB1mRNA and serum Cys C in DEXgroup were significantly decreased(P<0.05), and the histopathological damages in renal tissues were wellameliorated.ConclusionDexmedetomidine can effectivelyamelioratethe histopathologicaldamagesof therenal tissues in septic rats,and reduce the level of serum Cys C and theexpressions of HMGB1mRNAin renal tissues, showing protective effectsonsepsis-induced AKI. The mechanism of the renoprotection of dexmedetomidine may berelated to the expression of down-regulating HMGB1mRNA.