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陶涛, 付洁, 刘永刚等. 米诺环素抑制脑缺血再灌注后小胶质细胞激活的机制研究[J]. koko体育app 学报（医学版）, 2017, 48(2): 221-224.
引用本文: 陶涛, 付洁, 刘永刚等. 米诺环素控制脑梗死再灌入后小胶质細胞激发的工作机制研究方案[J]. 四川省高校学报（药学版）, 2017, 48(2): 221-224.
TAO Tao, FU Jie, LIU Yong-gang. et al. Minocycline Prevent Microglial Activation via Suppression of Adenosine A 2A Receptor in a Rat Stroke Ischemia/Reperfusion Model[J]. Journal of Sichuan University (Medical Sciences), 2017, 48(2): 221-224.
Citation: TAO Tao, FU Jie, LIU Yong-gang. et al. Minocycline Prevent Microglial Activation via Suppression of Adenosine A 2A Receptor in a Rat Stroke Ischemia/Reperfusion Model[J]. Journal of Sichuan University (Medical Sciences), 2017, 48(2): 221-224.

米诺环素抑制脑缺血再灌注后小胶质细胞激活的机制研究

Minocycline Prevent Microglial Activation via Suppression of Adenosine A 2A Receptor in a Rat Stroke Ischemia/Reperfusion Model

  • 摘要: 【摘要】 目的 观察米诺环素对大鼠脑缺血再灌注（ischemia/reperfusion，I/R）损伤后小胶质细胞的激活及神经炎症的影响，探讨腺苷A2A受体（adenosine A2Areceptor，A2AR）在米诺环素调节小胶质细胞活化中的作用机制。 方法 采用线栓法阻塞大脑中动脉制作大鼠I/R损伤模型，将30只SD大鼠随机分为假手术组、I/R模型组及米诺环素组〔I/R造模时，米诺环素按体质量3 mg/kg（质量浓度为100 g /1 mL）尾静脉注射，每日2次〕。再灌注24 h后，处死大鼠，取大鼠缺血侧脑组织，采用小胶质细胞特异性标记抗体CD11b/c染色、抗A2AR抗体免疫荧光以及双标染色检测缺血灶周围活化的小胶质细胞和A2AR蛋白的表达。Western blot法检测缺血脑组织内白介素-1β、-6（IL-1β、IL-6）及A2AR蛋白的表达。结果 I/R模型组CD11b阳性的小胶质细胞数明显多于假手术组；与I/R模型组相比，米诺环素组IL-1β、IL-6及A2AR蛋白表达下降（P <0.05），活化的小胶质细胞数目明显减少。结论 米诺环素可抑制局灶性脑I/R损伤所致的小胶质细胞激活及神经炎症反应，其机制可能与下调A2AR蛋白的表达有关。  
    Abstract: 【Abstract】 Objective To investigate whether minocycline could inhibit neuroinflammation induced by microglia activation through suppression of adenosine A2Areceptor (A2AR)expression in rats after cerebral ischemia/reperfusion (I/R) injury. Methods Thirty male Sprageue-Dawley rats were randomly divided into 3 groups: sham group, I/R group and minocycline group. The rats were subjected to occlusion of the right middle cerebral artery (MCAO) for 2 h to establish stroke I/R model, and 3 mg/kg minocycline was injected intravenously immediately after reperfusion twice a day in minocycline group. At 24 h after I/R, the inflammatory cytokines IL-1β and IL-6 in peri-infarct region were measured by Western blot, microglia activation was detected by double-immunofluorescence labeling. A2AR density was detected by immunohistofluorescence and Western blot. Results The number of CD11b-positive cells in I/R group was increased when compared with that in sham group. The expressions of IL-1β, IL-6 and A2AR were markedly up-regulated after I/R. Minocycline significantly decreased the expressions of IL-1β, IL-6 and A2AR and the number of CD11b-positive cells in peri-infarct region. Conclusion Minocycline could prevent cerebral ischemia induced neuroinflammation by the suppression of microglial activation, which may be related to down-regulation of A2ARexpression.  
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