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目的探讨艾芬地尔对脑缺血再灌注不同时相大鼠脑组织的保护作用及对Musashi1表达的影响。方法将84只Wistar大鼠随机分为3组,假手术组、脑缺血再灌注组(模型组)、艾芬地尔组(干预组)各28只,采用线拴栓塞法建立大脑中动脉闭塞模型,分别于再灌注2、3、7、14d各处死7只大鼠,其中1只用于透射电镜观察神经细胞超微结构变化,6只用于尼氏染色观察神经细胞组织学变化,免疫组化研究Musashi1的表达规律。结果 (1)与假手术组比较,模型组有以下表现,电镜:神经元胞体及细胞器肿胀明显,胞浆密度降低;尼氏染色:神经元数目减少,胞体肿胀,尼氏小体减少或消失;免疫组化:Musashi1阳性细胞在再灌注2d时即出现轻微增多,3d时表达急剧上升,持续至14d仍有较高表达;(2)与模型组比较,干预组表现特点如下,电镜:神经元胞体及细胞器轻度肿胀;尼氏染色:尼氏小体较多;免疫组化:Musashi1阳性细胞较相同时点模型组表达增多,光密度值增高,表达规律同模型组。结论艾芬地尔能够减轻脑缺血再灌注造成的细胞损伤,具有促进神经再生因子Musashi1表达的作用,对于改善脑缺血再灌注损伤具有积极作用。
Objective To investigate the protective effect of ifenprill on the brain tissue of rats with different phases of cerebral ischemia and reperfusion and its effect on Musashi1 expression. Methods Totally 84 Wistar rats were randomly divided into 3 groups: sham-operation group, cerebral ischemia-reperfusion group (model group) and Isoflurane group (intervention group), 28 rats in each group. The middle cerebral artery Occlusion model. Seven rats were sacrificed at 2, 3, 7 and 14 days after reperfusion, respectively. One of them was used to observe the ultrastructural changes of nerve cells by transmission electron microscopy. Six of them were used to observe the histological changes of nerve cells, Immunohistochemistry Musashi1 expression patterns. Results (1) Compared with the sham-operation group, the model group showed the following appearances: Electron microscopy: obvious swelling of cytoplasm and organelles of neurons and decrease of cytoplasm density; Nissl staining: the number of neurons decreased, somatic cell swelling and Nissl body reduced or disappeared ; Immunohistochemistry: Musashi1-positive cells showed a slight increase at 2 days after reperfusion, the expression rose sharply at 3d, and remained high up to 14 days. (2) Compared with the model group, the performance characteristics of the intervention group were as follows: Cell bodies and organelles mild swelling; Nissl staining: Nissl bodies more; Immunohistochemistry: Musashi1 positive cells increased compared with the model group at the same time point, the optical density increased, the expression of the same model group. Conclusions Allincin can relieve the cell injury induced by cerebral ischemia-reperfusion, promote the expression of Musashi1, and play an active role in improving cerebral ischemia-reperfusion injury.