丁苯酞对缺血脑组织RGMa表达及轴索损伤的影响

Effects of butylphthalide on RGMa expression and axonal injury in ischemic brain

目的:探讨丁苯酞对缺血性脑损伤后缺血脑组织排斥导向分子(RGMa)表达的影响。方法:120只成年雄性SD大鼠,随机分为假手术组,大脑中动脉闭塞(MCAO)模型组,生理盐水组,丁苯酞干预组。选取缺血后1h、3h、6h、12h、24h,进行神经功能评分,免疫组织化学观察RGMa的表达情况。结果:MCAO模型组、生理盐水组、丁苯酞组的改良的神经功能评分(mNSS)均高于假手术组,且随着时间的延长,mNSS评分越高;在缺血后3h、6h、12h、24h时,丁苯酞组的mNSS评分较MCAO模型组降低,差异具有统计学意义(P<0.05)。MCAO模型组、生理盐水组大鼠缺血后,不同时间点缺血区的RGMa蛋白阳性表达均有所增加,呈棕黄色染色。局灶性脑缺血后RGMa蛋白表达逐渐增多,在12h表达量最多;丁苯酞组在相应时间点的RGMa蛋白的表达较MCAO模型组有所降低,在6h、12h、24h时间点差异具有统计学意义。结论:丁苯酞可减少缺血性脑损伤大鼠的缺血脑组织的RGMa的表达,从而发挥神经功能保护作用。

Objective:To investigate the effect of butylphthalide on the expression of RGMa in ischemic brain.Methods:One hundred and twenty healthy male SD rats were randomly divided into following four groups:sham operation group,middle cerebral artery occlusion(MCAO)model group,saline group and the experimental group.Each group would be further divided into 5 subgroups(1 h,3 h,6 h,12 hand 24 h).The modified neurological severity scores and Western blot assay RGMa expression of ischemia side were performed at 1 h,3 h,6 h,12 h,24 hafter successful MCAO model.Results:The Modified Neurological Severity Score(mNSS)of MCAO model group,saline group,butylphthalide group were higher than those of sham group,mNSS were more higher as time went on;at 3 h,6 h,12 h,at 24 hafter ischemia,mNSS of NBP group compared with MCAO model group,the difference was statistically significant(P<0.05).After ischemia,RGMa protein expression of MCAO model group and saline group in ischemic area had increased,which were staining with brownish yellow.RGMa expression gradually increased as time went on,up to maximum at 12 h;RGMa protein expression of NBP group decreased,the difference between NBP group and MCAO group had statistically significant at 6 h,12 h,24 h;RGMa protein expression changes between cerebellum and ischemic area were similar,RGMa protein expression of NBP group were reduced,difference was statistically significant at 1 h,3 h,6 h,12 h(P<0.05).Conclusion:Butylphthalide can reduce the expression of RGMa in ischemic brain tissue of rats with ischemic brain,and thus has a neuroprotective role.