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目的探讨丁苯酞对脑梗死大鼠迁徙蛋白2(secreted leucine-rich repeat-containing protein 2,Slit2)表达的影响及其在脑梗死中的可能作用。方法 SD大鼠90只随机分为模型组、药物组和对照组各30只。模型组、药物组采用线栓法制备大鼠局灶性脑梗死模型,对照组颈总动脉不插入线栓;模型制备成功后,药物组给予丁苯酞120 mg/kg+花生油稀释至2 mL灌胃1次,模型组、对照组给予等量花生油灌胃。灌胃后1、3、7d,评定3组神经行为学评分,并分别处死10只大鼠,采用ELISA法检测3组脑组织Slit2表达水平。结果灌胃后1、3、7d,模型组神经行为学评分[(2.43±0.21)、(1.32±0.15)、(0.61±0.15)分]高于药物组[(1.50±0.24)、(0.41±0.12)、(0.03±0.01)分]和对照组[0、0、0分](P<0.05);灌胃后1、3、7d,药物组、模型组神经行为学评分逐渐降低;灌胃后1、3 d,药物组神经行为学评分高于对照组(P<0.05),灌胃后7 d与对照组比较差异无统计学意义(P>0.05);灌胃后1、3、7 d,药物组Slit2水平[(0.35±0.02)、(0.51±0.04)、(0.83±0.05)μg/L],模型组Slit2水平[(0.22±0.01)、(0.34±0.02)、(0.50±0.01)μg/L]高于对照组[(0.15±0.02)、(0.15±0.02)、(0.15±0.02)μg/L],且药物组Slit2水平高于模型组(P<0.05)。结论丁苯酞可能通过促进Slit2表达来减轻脑梗死大鼠脑损伤程度,促进脑功能恢复。
Objective To investigate the effect of butylphthalide on the expression of secreted leucine-rich repeat-containing protein 2 (Slit2) in cerebral infarction rats and its possible role in cerebral infarction. Methods Ninety SD rats were randomly divided into model group, drug group and control group, each with 30 rats. In the model group and the drug group, the focal cerebral infarction model was prepared by the method of thread plug, while the common carotid artery was not inserted in the control group. After the model was successfully prepared, the drug group was given the solution of butylphthalide 120 mg / kg + peanut oil diluted to 2 mL Stomach 1 time, the model group, the control group was given the same amount of peanut oil gavage. At 1, 3 and 7 days after gavage, the neurobehavioral scores of 3 groups were evaluated and 10 rats were sacrificed respectively. The expression of Slit2 was detected by ELISA in 3 groups. Results Compared with the drug group [(1.50 ± 0.24), (0.41 ± 0.24), (1.43 ± 0.21), (1.32 ± 0.15) and (0.61 ± 0.15) points respectively 0.12), (0.03 ± 0.01)] and control group [0,0,0 points] (P <0.05). On the 1st, 3rd and 7th day after administration, the neurobehavioral scores of the drug group and the model group decreased gradually; Neurological behavioral score of the drug group was significantly higher than that of the control group (P <0.05) at 1 and 3 days after treatment, and there was no significant difference between the drug group and the control group on the 7th day after gavage (P> 0.05) The levels of Slit2 in the model group were significantly higher than those in the model group (P <0.01) ) (μg / L) were significantly higher than those in the control group [(0.15 ± 0.02), (0.15 ± 0.02), (0.15 ± 0.02) μg / L] Conclusion Butylphthalide may reduce the brain injury and promote the recovery of brain function in rats with cerebral infarction by promoting the expression of Slit2.