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目的观察腺苷受体A2 a拮抗剂对大鼠MCAO模型纹状体中谷氨酸转运体GLT-1表达的影响,并探讨其对缺血性神经保护作用的机制。方法分别在雄性SD大鼠脑缺血2 h、缺血2 h再灌注22 h给予腺苷受体A2 a拮抗剂SCH-58261,采用RT-PCR、WB方法检测纹状体区GLT-1的表达,同时观察脑梗死体积和神经功能缺损情况。结果缺血2 h组的神经功能评分无明显差异;缺血2 h再灌注22 h干预组神经功能评分(1.67±0.52)与对照组(2.50±0.55)比较,有显著差异(P<0.05);缺血2 h干预组梗死体积(23.63±3.89),比对照组缩小了16%(P<0.05)。缺血2 h再灌注22 h干预组梗死体积(95.12±18.22),比对照组缩小了33%(P<0.01);给予SCH-58261后,MCAO大鼠在急性缺血期和缺血再灌注期纹状体中GLT-1表达均明显增高。结论初步证明阻断腺苷受体A2 a对脑缺血产生的保护作用与增强了GLT-1的功能有关。
Objective To investigate the effect of adenosine A2 receptor antagonist on glutamate transporter (GLT-1) in rat striatum and its mechanism of ischemic neuroprotection. Methods The adenosine A2 receptor antagonist SCH-58261 was induced in male Sprague-Dawley rats 2 h after cerebral ischemia and 22 h after ischemia and reperfusion, respectively. The expression of GLT-1 in striatum was detected by RT-PCR and WB Expression, while observing the volume of cerebral infarction and neurological deficits. Results There was no significant difference in neurological score between 2 h and 2 h after reperfusion, and there was a significant difference (P <0.05) between the neurological score (1.67 ± 0.52) and control group (2.50 ± 0.55) The volume of infarction in ischemic 2 h intervention group was 23.63 ± 3.89, which was 16% smaller than that in control group (P <0.05). The infarct volume in the intervention group (95.12 ± 18.22) at 2 h after ischemia and 2 h after ischemia was 33% smaller than that in the control group (P <0.01). After administration of SCH-58261, MCAO rats were sacrificed at acute ischemia and reperfusion The expression of GLT-1 in the striatum was significantly increased. Conclusions Preliminary evidence suggests that blockade of adenosine A2 receptor antagonizes the protective effects of cerebral ischemia and enhances the function of GLT-1.