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[米诺环素对大鼠局灶性脑缺血再灌注损伤后神经可塑性的影响]

[Effects of Minocycline on the Neuronal Plasticity in Rats after Focal Cerebral Ischemia Reperfusion Injury].

作者信息

Tao Tao, Qin Wen-yi, Li Zuo-xiao, Li Xiao-gang

出版信息

Sichuan Da Xue Xue Bao Yi Xue Ban. 2015 Jul;46(4):524-7.

PMID:26480651
Abstract

OBJECTIVE

To observe the effects of minocycline on morphology and the expression of synaptophysin in cortical tissues of rats after cerebral ischemia reperfusion injury.

METHODS

36 male SD rats were randomly divided into 3 groups: sham group, model group [ischemia reperfusion (I/R)] and minocycline (Min) group (treated with minocycline for 14 d, 3 mg/kg, 2 times/d ). Middle cerebral artery occlusion (MCAO) was used to established as focal cerebral I/R model. At 14 d after I/R. Neurological functional recovery was evaluated using the staircase test, the cell morphology in cortex was evaluated by HE staining, the neurite growth was observed by immunostaining with anti-microtubule-associated protein-2 (MAP-2) antibody, the expression of synaptophysin in pei-infarct region was tested by Western blot.

RESULTS

In the sham group, the rats did not show any neurological deficits. The neurons in the cortex were arranged in neat rows and the morphology were normal, the MAP-2 positive neurons showed longer neuronal processes than the model group. Compared to the model group, minocycline significantly improved forelimb motor function, increased the expression of synaptophysin and the number of MAP-2-positive cells in peri-infarct region (P < 0.05).

CONCLUSION

Minocycline could improve the neurite regrowth and the expression of synaptophysin of neuron in ischemic cortex, promote neurological functional recovery of rats after MCAO, which is related to regulate the neuronal plasticity.

摘要

目的

观察米诺环素对脑缺血再灌注损伤大鼠皮质组织形态及突触素表达的影响。

方法

将36只雄性SD大鼠随机分为3组:假手术组、模型组[缺血再灌注(I/R)组]和米诺环素(Min)组(给予米诺环素治疗14天,3mg/kg,每日2次)。采用大脑中动脉闭塞(MCAO)法建立局灶性脑I/R模型。I/R后14天,采用阶梯试验评估神经功能恢复情况,通过HE染色评估皮质细胞形态,用抗微管相关蛋白-2(MAP-2)抗体免疫染色观察神经突生长情况,采用蛋白质印迹法检测梗死周边区突触素的表达。

结果

假手术组大鼠未出现任何神经功能缺损。皮质神经元排列整齐,形态正常,MAP-2阳性神经元的神经突比模型组更长。与模型组相比,米诺环素显著改善前肢运动功能,增加梗死周边区突触素的表达及MAP-2阳性细胞数量(P<0.05)。

结论

米诺环素可促进缺血皮质神经元神经突再生及突触素表达,促进MCAO大鼠神经功能恢复,这与调节神经元可塑性有关。

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