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目的观察丁苯酞(NBP)对大鼠脑缺血再灌注损伤后脑组织Bim蛋白表达的影响。方法将24只雄性SD大鼠随机分为假手术组、模型组和实验组,每组8只。模型组和实验组用线栓法制作大鼠大脑中动脉脑缺血再灌注模型,假手术组接受相似手术处理,但是不插入线栓。实验组于大脑中动脉栓塞后15 min内灌胃予以80 mg·kg~(-1)丁苯酞,给药一次;模型组和假手术组予以相同体积的食用麻油,给药一次。用TUNEL染色法原位检测各组大鼠缺血侧皮质区神经元细胞凋亡情况,用免疫组织化学法和Western blot法检测各组大鼠缺血侧皮质区Bim蛋白表达情况。结果与假手术组(16.36±3.29)相比,模型组和实验组缺血侧皮质区神经元细胞凋亡程度分别为(89.42±12.68)和(56.38±8.71),差异均有统计学意义(P<0.05)。与假手术组(0.13±0.03)相比,模型组和实验组缺血侧皮质区Bim蛋白表达水平分别为(0.82±0.14)和(0.64±0.08),差异均有统计学意义(P<0.05)。实验组和模型组的缺血侧皮质区神经元细胞凋亡程度、Bim蛋白表达水平比较差异均有统计学意义(P<0.05)。结论丁苯酞能抑制大鼠脑缺血再灌注损伤后的神经细胞凋亡,其机制可能与抑制Bim蛋白的表达有关。
Objective To observe the effect of butylphthalide (NBP) on the expression of Bim protein in brain tissue after cerebral ischemia-reperfusion injury in rats. Methods Twenty-four male SD rats were randomly divided into sham operation group, model group and experimental group, with 8 rats in each group. The model group and the experimental group were given middle cerebral artery occlusion (MCAO) cerebral ischemia and reperfusion model by the method of thread occlusion. The sham operation group received similar surgical treatment but did not insert the thread plug. In the experimental group, butylphthalide (80 mg · kg -1) was given intragastrically within 15 min after embolization of the middle cerebral artery and administered once. The same volume of sesame oil was administered to the model group and the sham operation group once a day. The apoptosis of neurons in ischemic cortex of rats in each group was detected by TUNEL staining in situ. The expression of Bim protein in ischemic cortex of rats in each group was detected by immunohistochemistry and Western blot. Results Compared with the sham operation group (16.36 ± 3.29), the apoptotic rates of neurons in the ischemic cortex of the model group and the experimental group were (89.42 ± 12.68) and (56.38 ± 8.71), respectively, with statistical significance ( P <0.05). Compared with the sham group (0.13 ± 0.03), the Bim protein expression in the ischemic cortex of model group and experimental group were (0.82 ± 0.14) and (0.64 ± 0.08) respectively, the difference was statistically significant (P <0.05 ). The degree of neuron apoptosis and the expression of Bim protein in ischemic cortex of experimental group and model group were significantly different (P <0.05). Conclusion Butylphthalide can inhibit neuronal apoptosis after cerebral ischemia-reperfusion injury in rats, which may be related to the inhibition of the expression of Bim protein.