中文摘要：

目的评价吗啡延迟预处理对小鼠缺血性脑损伤的影响及经典型蛋白激酶c（cPKc）在其中的作用。方法雄性BALB／C小鼠40只，体重20～22g，采用随机数字表法，将其分为4组（n=10）：假手术组（s组）、缺血性脑损伤组（ICI组）、吗啡延迟预处理组（MP组）和cPKC抑制剂G06983组（G组）。采用大脑中动脉阻塞法制备缺血性脑损伤模型。MP组于模型制备前24h时腹腔注射吗啡10mg／kg；G组于模型制备前24h时腹腔注射吗啡10mg／kg，并于模型制备前即刻侧脑室注射5μl G06983（6nm01）。模型制备后6h时，进行神经功能缺陷评分，随后处死小鼠，取脑组织，测定脑水肿率和梗死体积，计算细胞凋亡率。结果与s组相比，ICI组、MP组和G组神经功能缺陷评分、脑梗死体积、水肿率和细胞凋亡率升高（P〈0．01）；与ICI组相比，MP组神经功能缺陷评分、脑梗死体积、水肿率和细胞凋亡率降低（P〈0．01），G组上述指标差异无统计学意义（P〉0．05）。结论吗啡延迟预处理可减轻小鼠缺血性脑损伤，机制与激活cPKC信号通路有关。

英文摘要：

Objective To evaluate the effect of delayed preconditioning with morphine on ischemic cere- bral injury in mice and the role of classical protein kinase C （cPKC） . Methods Forty male BALB/C mice, weigh- ing 20-22 g, were randomly divided into 4 groups （ n = 10 each） ： sham operation group （group S）, ischemic ce- rebral injury group （group ICI）, morphine preconditioning group （group MP） and cPKC inhibitor Go6983 group （group G）. Ischemia was induced by middle cerebral artery occlusion （MCAO） . In S group, the middle cerebral artery was only exposed but not occluded. In MP group, morphine 10 mg/kg was injected intraperitoneally 24 h be- fore MCAO. In G group, morphine 10 mg/kg was injected intraperitoneally 24 h before MCAO and 5 μl Go6983 （6 nmol） was injected into the left lateral cerebral ventricle immediately before MCAO. The neurologic deficit was evaluated and scored according to neurological disability status scale in a blind manner 6 h after MCAO. The ani- mals were sacrificed and brains were immediately removed for measurement of the brain edema and infarct volume. Apoptotic rate was calculated. Results Compared with S group, the neurologie deficit scores, infarct volume, brain edema and apoptotic rate were significantly increased in ICI, MP and G groups （P 〈 0.01 ）. Compared with group ICI, the neurologic deficit scores, infarct volume, brain edema and apoptotic rate were significantly de- creased in group MP （ P 〈 0.01 ）, and no significant change was found in the parameters mentioned above in group G （ P 〉 0.05） . Conclusion Delayed preconditioning with morphine can reduce ischenfie cerebral injury in mice and activation of classical cPKC signaling pathway is involved in the mechanism.