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目的探讨阻断腺苷A2A受体对神经元缺血性损伤的影响及其可能机制。方法将腺苷A2A受体基因敲除(A2ARKO)小鼠24只及同窝野生型(A2ARWT)小鼠24只分为A2ARKO组和A2ARWT组,每组下设脑缺血2h(各6只)、脑缺血后再灌注22h(各6只)和脑缺血后再灌注46h(各12只)3个时相点,另外9只A2ARWT小鼠设为假手术组。线栓法制作大脑中动脉阻塞(middle cerebral artery occlusion,MCAO)模型,脑组织切片甲酚紫染色结合图象分析技术测定脑梗死体积,干湿质量法测定脑组织含水量,免疫组化染色检测钙结合蛋白(Calbindin D-28k,CB)和水通道蛋白4(aquaporin,AQP4)。结果在脑缺血2h、脑缺血后再灌注22h和脑缺血后再灌注46h,测定A2ARKO组的脑梗死体积均小于A2ARWT组的梗死体积;与A2ARWT组比较,A2ARKO组脑内CB表达较多,AQP4表达较少,脑含水量较低。结论阻断腺苷A2A受体对脑缺血急性期和再灌注期损伤均有保护作用,并减轻缺血引起的脑水肿,可能与抑制细胞内钙超载和AQP4的表达有关。
Objective To investigate the effect of adenosine A2A receptor block on neuronal ischemic injury and its possible mechanism. Methods Twenty-four A2AR A2 mice and A2ARWT mice were divided into two groups: A2ARKO group and A2ARWT group. Each group was divided into 2 groups (6 rats in each group) , Reperfusion after cerebral ischemia 22h (each 6) and reperfusion after cerebral ischemia 46h (12 each) three time points, and the other 9 A2ARWT mice were set as sham operation group. The MCAO model was made by the method of thread occlusion. The volume of cerebral infarction was determined by cresyl violet staining of brain tissue and the image analysis technique. The water content of brain tissue was measured by wet and dry mass method. Calbindin D-28k (CB) and aquaporin 4 (AQP4). Results Cerebral infarction volume in A2ARKO group was lower than that in A2ARWT group at 2h after cerebral ischemia, 22h after reperfusion after cerebral ischemia and 46h after reperfusion after cerebral ischemia. Compared with A2ARWT group, More, AQP4 expression less brain water content is lower. Conclusions Blockade of adenosine A2A receptor has a protective effect on acute cerebral ischemia and reperfusion injury, and reduces cerebral edema induced by ischemia, which may be related to the inhibition of intracellular calcium overload and the expression of AQP4.