【摘要】 目的 探讨“中风1号”通过激活PI3K/Akt信号通路，抑制GSK-3β蛋白表达，减少神经细胞凋亡、减轻脑出血后神经功能损伤机制。方法 将SD雄性大鼠40只随机分为假手术组、模型组、中风1号组、甘露醇组，每组10只。评估大鼠术后24 h、3 d、7 d神经功能评分，Western blotting检测PI3K、Akt、GSK-3β蛋白表达水平。结果 各组大鼠术后24 h（给药前），模型组与假手术组比较（P <0.05），造模成功。术后3、7 d，模型组与假手术组比较神经功能评分明显升高（P <0.05），中风1号组、甘露醇组分别与模型组比较，评分明显降低（P <0.05）。与假手术组相比，模型组PI3K、Akt蛋白表达显著降低（P <0.05）,GSK-3β蛋白表达显著增高（P <0.05）。与模型组相比，中风1号组、甘露醇组PI3K、Akt蛋白表达均显著上升（P <0.05）,GSK-3β蛋白表达显著下降（P <0.05）。结论“中风1号”可减轻脑出血后神经细胞凋亡、改善脑出血后神经功能损伤，其机制与PI3K/Akt信号通路、GSK-3β蛋白表达有关。更多还原

【Abstract】 Objective:To explore the mechanism of "Zhongfeng No.1" by activating the PI3K/Akt signaling pathway,inhibiting the expression of GSK-3β protein,reducing neuronal apoptosis and reducing neurological damage after cerebral hemorrhage. Methods:A total of 40 SD male rats were randomly divided into the sham operation group,model group, "Zhongfeng No.1" group,and mannitol group,with 10 rats in each group. The neurological function scores of rats at 24 h(before administration),3,and 7 d were evaluated,and the expression levels of PI3K,Akt,and GSK-3β protein were detected by Western blotting. Results:Rats in each group were successfully modeled 24 h after the operation(before administration). The model group was compared with the sham operation group(P < 0.05). At 3 and 7 d after operation,the scores of the model group was significantly higher than the sham operation group(P < 0.05),and the scores of the "Zhongfeng No.1" group and the mannitol group were significantly lower than the model group(P < 0.05). Western blotting detection results showed that compared with the sham operation group,the expression of PI3K and Akt protein in the model group was significantly reduced(P <0.05),and the expression of GSK-3β protein was significantly increased(P < 0.05). Compared with the model group,the expression of PI3K and Akt protein in the "Zhongfeng No.1" group and the mannitol group were significantly increased(P < 0.05),and the expression of GSK-3β protein was significantly decreased(P < 0.05). Conclusion: "Zhongfeng No.1" can reduce neuronal apoptosis and improve neurological damage after cerebral hemorrhage. The mechanism is related to the PI3K/Akt signaling pathway and the expression of GSK-3β protein.更多还原