Objective To investigate the mechanism of preconditioning on renal ischemia reperfusion injury in rats and the effects of dexmedetomidine under high glucose condition .Methods From October 2014 to June 2015 , in the Central Laboratory of Renmin Hospital of Wuhan University , 36 adult male SD rats were randomly divided into:sham operation group (NG-sham), ischemia and reperfusion group (NG-I/R) and dexmedetomidine preset treatment group (NG-Dex), high glu-cose sham operation group ( HG-Sham) , sugar ischemia again perfusion group ( HG-I/R) , high glucose dexmedetomidine pre-set treatment group (HG-Dex) with 6 rats in each group.The renal ischemia reperfusion model was made in all groups except the sham operation group , Dex pretreatment group was injected Dex 50μg/kg 30 min before ischemia .Cell apoptosis was de-termined by in situ terminal transferase labeling (TUNEL) method.Blot Western method was used to detect Bax , Bcl-2, pro-tein kinase B (AKT) and phosphorylated AKT (p-AKT).Results Compared with NG Sham group, NG-I/R group can be seen in tubular damage obviously , including renal tubular expansion , renal tubular epithelial cell swelling , nucleus proprius and inflammatory renal tubular necrosis , apoptosis index, Bax, p-AKT were increased, Bcl 2 was decreased ( F =6.667, F =469.889, F =1.200, F =0.791, F =0.499, P <0.05);compared with NG I/R group, NG-Dex group structure was normal, visible to the normal structure of renal tubule and renal tubular cells , apoptosis index and Bax decreased , and p-AKT, Bcl-2 increased ( F =59.333, F =27.667, F =0.028, F =0.034, F =0.024, P <0.05); HG-I/R group, HG-Dex cell damage the degree of apoptosis index , Bax, p-AKT were higher than that of NG I/R group and NG-Dex group, the Bcl 2 lower than that of the corresponding group ( F =66.000, F =497.556, F =1.227, F =0.824, F =0.523, P <0.05); HG-I/R group, HG group's p-AKT Dex apoptosis index had no significant difference ( P >0.05).Conclusion Dex has a protective effect on normal renal ischemia-reperfusion injury , but this effect is impaired in a high glucose environment , which may be related to the expression of p-AKT, regulation of Bcl-2 and Bax, and increased renal I/R damage.%目的：探讨高糖状态下右美托咪定（ Dex）预处理对大鼠肾缺血再灌注损伤影响的机制。方法2014年10月—2015年6月于武汉大学人民医院中心实验室进行实验，成年雄性SD大鼠36只随机分为：假手术组（ NG-Sham）、缺血再灌注组（NG-I／R）、右美托咪定预处理组（NG-Dex）、高糖假手术组（HG-Sham）、高糖缺血再灌注组（HG-I／R）、高糖右美托咪定预处理组（HG-Dex）各6只。除假手术组外其余各组均制备肾缺血再灌注模型，Dex预处理组于缺血前30 min腹腔注射Dex 50μg／kg。采用原位末端转移酶标记（TUNEL）法测定细胞凋亡，Western blot法检测肾脏Bax、Bcl-2、蛋白激酶B（ AKT）、磷酸化AKT（ p-AKT）。结果与NG-Sham组比较，NG-I／R组可见到明显的肾小管损害，包括肾小管扩张，肾小管上皮细胞肿胀，固有核，炎性肾小管坏死，凋亡指数、Bax、p-AKT均增高，而Bcl-2降低（ F ＝6创．667、469．889、1．200、0．791、0．499， P ＜0．05）；与NG-I／R组比较，NG-Dex组结构较为正常，可见到正常的肾小管结构和肾小管细胞，凋亡指数、Bax降低，而p-AKT，Bcl-2升高（ F ＝59．333、27．667、0．028、0．034、0．024， P ＜0．05）；HG-I／R组、HG-Dex组的细胞破坏程度、凋亡指数、Bax、p-AKT分别高于对应的NG-I／R组、NG-Dex组，而Bcl-2低于对应组（ F ＝66．000、497．556、1．227、0．824、0．523， P ＜0．05）；HG-I／R组、HG-Dex组之间凋亡指数、p-AKT无明显差异（ P ＞0．05）。结论 Dex对正常肾缺血再灌注损伤具有保护作用，但这种作用在高糖环境中被削弱，可能与通过p-AKT、调控Bcl-2及Bax的表达，进而增加肾I／R损伤有关。
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