目的 通过观察腺苷预处理对脑缺血-再灌注（IR）损伤后大鼠脑内肿瘤坏死因子α（TNF-α）和核因子κB（NF-κB）表达的影响，探讨腺苷对大鼠脑缺血-再灌注损伤的保护机制。  方法 Sprague-Dawley大鼠60只随机分为假手术组（F组）、缺血-再灌注组（IR组）和腺苷预处理缺血-再灌注组（AP组），每组动物按照缺血-再灌注后2 h、6 h、24 h及48 h这4个时间点随机分组，每组5只。采用大脑中动脉阻塞（MCAO）法制备大鼠大脑中动脉闭塞模型。通过对以上3组脑缺血再灌注48 h后的大鼠脑组织行头颅MRI、HE染色以及对以上60只大鼠进行神经功能缺损评分，通过免疫组织化学方法观察大鼠脑组织中TNF-α和NF-κB的平均积分吸光度值进一步验证腺苷预处理对大鼠脑缺血-再灌注损伤的脑保护作用，探讨腺苷对大鼠脑缺血-再灌注损伤的保护机制。  结果 F组大鼠术后无神经功能缺损体征，AP组和IR组大鼠术后均出现明显神经功能缺损体征。AP组和IR组大鼠神经功能缺损评分显著高于F组，AP组大鼠神经功能缺损评分显著低于IR组，差异均具有统计学意义（P＜0.05）。F组大鼠术后MRI中T1WI、T2WI均未见明显异常，AP组和IR组大鼠脑梗死体积显著高于F组，AP组大鼠脑梗死体积显著低于IR组，差异均具有统计学意义（P＜0.05）。AP组和IR组术后大鼠脑组织中TNF-α和NF-κB的表达显著高于F组，AP组术后大鼠脑组织中TNF-α和NF-κB的表达显著低于IR组，差异均具有统计学意义（P＜0.05）。  结论 腺苷预处理可通过减少大鼠缺血-再灌注损伤后脑内TNF-α和NF-κB的表达而减轻神经细胞损伤，达到其脑保护作用。

Objective To observe the effect of adenosine preconditioning on the expression of tumor necrosis factor α（TNF-α）and nuclear factor κB (NF-κB)in rats after cerebral ischemia-reperfusion(IR) injury,and to explore the protective mechanism of adenosine on focal cerebral ischemia-reperfusion injury in rats.   Methods Total sixty Sprague-Dawley rats were randomly divided into sham group (F group),ischemia-reperfusion group (IR group) and adenosine preconditioning ischemia-reperfusion group (AP group). Each group was randomly divided into 5 mice at 2 hour, 6 hour, 24 hour and 48 hour after ischemia-reperfusion. The rat moadel of middle cerebral artery occlusion (MCAO) was established by suppository method . 48 hours after ischemia-reperfusion, line head MRI, HE staining and for more than of 60 neursl function defect scale in rats，integral optical density of the software system by immunohistochemical method  in the observation group rats TNF-α and NF-κB average absorbance values of rats’brain tissues to further verify the adenosine preconditioning on rat cerebral ischemia-reperfusion injury，adenosine on rat focal cerebral ischemia-reperfusion injury of protection mechanism.  Results No signs of neurological defects was found in the rats in F after surgery, and obvious signs of neurological defects were found in the rats of AP and IR groups.The neurological defect scores of the AP group and the IR group were significantly higher than those of the F group, and the neurological defect scores of the AP group were significantly lower than those of the IR group, with statistically significant differences(P<0.05).Postoperative MRI images of T1WI and T2WI of rats in group F showed no obvious abnormalities. The cerebral infarction volume of rats in the AP group and the IR group was significantly higher than those of the F group, and the cerebral infarction volume of rats in the AP group was significantly lower than those of the IR group,with statistically significant differences(P<0.05).The expressions of TNF-α and NF-κB in the brain tissues of the AP group and the IR group were significantly higher than those of the F group, and the expressions of TNF-α and NF-κB in the brain tissues of the AP group was significantly lower than those of the IR group, with statistically significant differences(P<0.05).   Conclusion Adenosine preconditioning can protect the brain by descreasing the expression of TNF-α and NF-κB in rats with cerebral ischemia-reperfusion injury.