盐酸右美托咪定对糖尿病大鼠术后认知功能障碍及炎症反应的影响

Effects of dexmedetomidine on postoperative cognitive dysfunction and inflammatory response in diabetic rats

目的探究盐酸右美托咪定(Dex)对糖尿病大鼠术后认知功能障碍(POCD)的影响及其作用机制。方法选择成年健康的雄性SD大鼠60只,予其腹腔注射链脲佐菌素(STZ)50mg/kg,72h后于大鼠尾静脉采血检测空腹血糖,空腹血糖在1周内持续≥16.7mmol/L则造模成功。在造模成功的糖尿病大鼠中随机选取40只进行脾切除术,使用CHISS统计学软件将其随机分为A组(n=20,尾静脉穿刺泵注生理盐水)与B组(n=20,尾静脉穿刺泵注Dex)。记录大鼠术前、术后的空腹血糖,手术结束后,在各组存活大鼠中随机选取10只进行行为学检测并检测其海马区的TNF-α及IL-1β水平。结果术后,A组大鼠空腹血糖水平明显高于B组(P<0.05)。B组大鼠同一时间的平均逃避潜伏期明显短于A组(P<0.05)。B组大鼠游泳时间百分比高于A组,穿越次数多于A组(P<0.05)。B组大鼠海马区TNF-α及IL-1β水平均低于A组(P<0.05)。结论Dex可以改善糖尿病大鼠POCD,其机制可能与减轻海马区的炎症反应有关。

Objective To investigate the effect and mechanism of dexmedetomidine(Dex)on postoperative cognitive dysfunction(POCD)in diabetes rats.Methods Sixty adult healthy male SD rats were intraperitoneal injection with streptozotocin(STZ)50 mg/kg.Fasting blood glucose was measured in caudal vein of rats after 72 hours.The model was successfully established when fasting blood sugar lasted for more than 16.7 mmol/L within one week.Forty rats who were successfully established diabetes were randomly selected for splenectomy and randomly divided into group A(n=20,physiological saline was pump injected by tail vein puncture)and group B(n=20,Dex was pump injected by tail vein puncture).Fasting blood glucose was recorded before and after operation.After operation,10 cases surviving rats in each group were randomly selected for behavioral testing and the levels of TNF-αand IL-1βin hippocampus were detected.Results After operation,the level of fasting blood glucose in the group A was significantly higher than that in the group B(P<0.05).The average escape latency in the group B at the same time was significantly shorter than that in the group A(P<0.05).The percentage of swimming time in the group B was higher than that in the group A,and the number of times of swimming was more than that in the group A(P<0.05).The levels of TNF-αand IL-1βin hippocampus in the group B were lower than those in the group A(P<0.05).Conclusion Dex can improve POCD in diabetes rats.The mechanism may be related to reduce the inflammatory response in the hippocampus.