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目的探讨丁苯酞对缺血性脑白质损害的影响及丁苯酞对缺血性白质损害的干预效果。方法雄性Wistar大鼠30只,随机分为对照组、缺血组和治疗组,每组10只。缺血组和治疗组给予双侧颈总动脉结扎,对照组给予假手术处理;术后治疗组给丁苯酞腹腔注射,对照组和缺血组给予生理盐水腹腔注射。术后1个月评测各组大鼠脑白质区HE及免疫组化染色观察到神经元、胶原纤维酸性蛋白(GFAP)性细胞数目及髓鞘碱性蛋白(MBP)的变化。结果缺血组大鼠脑深部白质区可见神经元数目较对照组明显减少且排列稀疏紊乱,GFAP阳性细胞数目较对照组及治疗组明显增多(P<0.05),缺血组MBP的灰度值较对照组及治疗组下降,三者之间差异有统计学意义(P<0.05)。结论丁基苯酞可改善慢性缺血大鼠白质损害。
Objective To investigate the effect of butylphthalide on ischemic white matter damage and the effect of butylphthalide on ischemic white matter damage. Methods Thirty male Wistar rats were randomly divided into control group, ischemia group and treatment group, with 10 rats in each group. Bilateral common carotid arteries were ligated in the ischemic group and the treatment group, and sham-operated in the control group. Butylphthalide was injected intraperitoneally in the postoperative treatment group and normal saline in the control group and ischemia group. One month after operation, the number of neurons, the number of glial fibrillary acidic protein (GFAP) cells and the change of myelin basic protein (MBP) were observed by HE staining and immunohistochemistry in white matter of rats in each group. Results Compared with the control group, the number of neurons in the deep white matter of the ischemic group was significantly decreased and sparsely arranged. The number of GFAP positive cells in the ischemic group was significantly higher than that in the control group and the treated group (P <0.05). The gray value of MBP in the ischemic group Compared with the control group and the treatment group decreased, the difference between the three was statistically significant (P <0.05). Conclusion Butylphthalide can improve the white matter damage in chronic ischemic rats.