运动训练对大鼠局灶脑梗死后脑内LINGO-1的表达及其对神经功能的影响

Effects of exercise training on expressions of LINGO-1 in the brain of rats and neural function after focal cerebral infarction

摘要:

目的：观察大鼠运动训练后脑内LINGO-1表达的变化，从而揭示运动训练促进脑卒中后神经功能恢复的可能分子机制。方法：采用线栓法制备大脑中动脉闭塞（middle cerebralartery occlusion，MCAO）模型，随机将大鼠分为假手术组、模型组及运动训练组，选取3、7、14 d 3个时间点观察，运动训练采用跑台跑步方法。运用Longa评分进行神经功能评价，RT-PCR进行 LINGO-1 mRNA检测，免疫组织化学观察LINGO-1蛋白水平变化。结果：假手术组无明显神经功能缺损，Longa评分0分，其 LINGO-1 mRNA及蛋白水平有少量阳性表达。模型组LINGO-1表达3 d为高峰，后逐渐降低（P<0.05）。运动训练组与模型组相比，在3 d及7 d时间点Longa评分、mRNA及蛋白水平表达无明显差异（P >0.05），在14 d时间点Longa评分、LINGO-1 mRNA 及蛋白水平均有下降（P<0.05）。结论：局灶性脑梗死后大鼠脑内LINGO-1水平明显上调，适当时间的运动训练可降低LINGO-1的表达水平及神经功能评分，这可能是运动训练促进脑梗死后神经功能恢复的分子机制之一。

Abstract:

Objective：To observe the expressions of LINGO-1 in the brain of rats after exercise training and to explore the possible molecular mechanism of exercise training promoting neurological functional recovery after stroke. Methods：Middle cerebral artery oc－clusion（MCAO） model was made and rats were randomly divided into sham operation group，model group and exercise training group. Observation was made at 3，7，14 d after MCAO. Training method was treadmill exercise. Neurological functional recovery was evalu－ated by Longa’s score；expressions of LINGO-1 mRNA and protein were detected by imunohistochemistry and RT-PCR. Results：Sham group had no obvious neurological deficiency（Longa score was 0） but small amount of mRNA and protein expressions of LIN－GO-1. mRNA and protein expressions of LINGO-1 in model group were reached the peak at 3 d after MCAO and decreased gradual－ly later（P<0.05）. There was no difference in mRNA and protein expressions of LINGO-1 between exercise training group and model group at 3，7 d after MCAO（P >0.05）. Longa score and mRNA and protein expressions of LINGO-1 were decreased at 14 d after MCAO in exercise training group compared with those in model group（P<0.05）. Conclusions：Expressions of LINGO-1 in the is－chemic brain are increased significantly. Decreased neurological score and LINGO-1 mRNA and protein expressions induced by prop－er exercise training might be one of the molecular mechanisms of neural function recovery after acute cerebral infarction.