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目的探讨三七皂苷Rg1对脑缺血损伤后大鼠大脑皮质、小脑和延髓Bcl-2、Bax蛋白表达的影响。方法 SD雄性大鼠随机分为6组,即假手术组、模型组、阳性对照组、三七皂苷Rg1低(25 mg/kg)、中(50 mg/kg)和高(100 mg/kg)剂量组。除假用术组外,其余组采用线栓法复制大鼠大脑中动脉阻塞再灌注模型,每天给药2次。假手术组和模型组给予等体积的生理盐水,阳性对照组给予尼莫地平(1 mg/kg),三七皂苷Rg1各组给予相应剂量的三七皂苷Rg1,均按5 mL/kg的容量腹腔注射。给药24 h后采用神经缺失症状评分法和动物死亡率,处死动物后采用免疫组化法分别检测大鼠大脑皮质、小脑和延髓Bcl-2、Bax蛋白的表达情况。结果三七皂苷Rg1各组大鼠脑缺血损伤后的死亡率和神经缺失评分明显降低,大鼠大脑皮质、小脑和延髓Bcl-2与Bax蛋白表达的比值增加,与模型组比较差异有统计学意义(P<0.05,P<0.01),除大脑皮质Bcl-2与Bax蛋白的比值外,三七皂苷Rg1的中剂量与低剂量比较差异有统计学意义(P<0.05)。在神经缺失症状评分和动物死亡率方面,三七皂苷Rg1的中、高剂量组与阳性对照组比较差异有统计学意义(P<0.05,P<0.01);在大脑皮质和延髓Bcl-2/Bax方面,三七皂苷Rg1各剂量组与阳性对照组比较均差异有统计学意义(P<0.05,P<0.01);在小脑的Bcl-2/Bax方面,只有三七皂苷Rg1中剂量组与阳性对照组比较差异有统计学意义(P<0.05)。结论三七皂苷Rg1抗脑缺血损伤的作用机制与其增加大鼠大脑皮质、小脑和延髓的Bcl-2蛋白表达,降低大鼠大脑皮质和延髓的Bax蛋白表达及上调Bcl-2与Bax的比值有关。
Objective To investigate the effect of notoginsenoside Rg1 on the protein expressions of Bcl-2 and Bax in the cerebral cortex, cerebellum and medulla oblongata after cerebral ischemia. Methods SD male rats were randomly divided into 6 groups: sham operation group, model group, positive control group, low (25 mg / kg), medium (50 mg / kg) and high (100 mg / Dose group. Except the sham-operation group, the other groups were subjected to occlusion-reperfusion model by middle cerebral artery occlusion (MCAO) by thread occlusion method. The model was administered twice a day. The sham operation group and model group were given equal volume of normal saline, the positive control group was given nimodipine (1 mg / kg), and the notoginsenoside Rg1 group was given the corresponding dose of notoginsenoside Rg1, according to the volume of 5 mL / kg Intraperitoneal injection. The neurological deficit symptom score and animal mortality were measured 24 h after drug administration. The expression of Bcl-2 and Bax protein in cerebral cortex, cerebellum and medulla oblongata was detected by immunohistochemistry after the animals were sacrificed. Results The percentages of death and nerve deficits after cerebral ischemia injury were significantly decreased in each group of notoginsenoside Rg1. The ratio of Bcl-2 and Bax in cerebral cortex, cerebellum and medulla oblongata increased significantly compared with the model group (P <0.05, P <0.01). Except for the ratio of Bcl-2 and Bax protein in cerebral cortex, there was significant difference between low dose and medium dose of notoginsenoside Rg1 (P <0.05). In the neurological deficit symptom score and animal mortality rate, the middle and high doses of notoginsenoside Rg1 were significantly different from the positive control group (P <0.05, P <0.01); in the cerebral cortex and medulla oblongata Bcl-2 / Bax, all the doses of notoginsenoside Rg1 had significant difference compared with the positive control group (P <0.05, P <0.01); in the cerebellum Bcl-2 / Bax, only the notoginsenoside Rg1 middle dose group Positive control group, the difference was statistically significant (P <0.05). Conclusion The mechanism of action of notoginsenoside Rg1 on cerebral ischemia injury is related to the increase of Bcl-2 protein expression in rat cerebral cortex, cerebellum and medulla oblongata, the decrease of Bax protein expression in cerebral cortex and medulla oblongata, and the up-regulation of Bcl-2 and Bax ratio related.