目的 毛蕊异黄酮对 H2O2诱导的氧化损伤的星形胶质细胞增殖和凋亡的影响。方法 分 离 SD 新生大鼠星形胶质细胞；分别用 5、10、20 μmol/L 的毛蕊异黄酮作用星形胶质细胞 12 h 后，加入 H2O2 处理 24 h 造成氧化损伤模型，用 CCK8 法检测各组细胞增殖情况以筛选合适的毛蕊异黄酮处理浓度；实验 分为对照组、H2O2 （100 μmol/L）模型组、H2O2 （100 μmol/L）+毛蕊异黄酮（20 μmol/L）干预组；用 CCK8 法 观察对星形胶质细胞增殖的影响；流式细胞术检测细胞凋亡情况；免疫荧光检测各组样本中 Brdu 水平； Western blot 检测各组细胞中 p⁃AKT、GP130、IL⁃6 蛋白表达。结果 与对照组相比，H2O2组的星形胶质细 胞增殖活力降低，细胞凋亡程度加重，p⁃AKT、GP130、IL⁃6 蛋白表达量均显著升高（P < 0.05）；在毛蕊异黄 酮干预后，星形胶质细胞增殖活力明显上升，并能有效抑制细胞凋亡，下调 p⁃AKT、GP130、IL⁃6 蛋白表达 量（P < 0.05）。结论 毛蕊异黄酮可以通过抑制 PI3K/Akt 信号通路磷酸化促进 H2O2诱导的氧化损伤的星 形胶质细胞的增殖，并抑制其凋亡。

Objective To investigate the effect of rissoflavones on proliferation and apoptosis of H2O2 ⁃ induced oxidative damage⁃induced astrocyte. Methods Astrocytes of SD neonatal rat were isolated；after treating astrocytes with 5，10，20 μmol/L isoflavones for 12 h，and adding H2O2 for 24 h to induce oxidative damage model， the cell proliferation in each group was detected by CCK8 method. In order to screen the appropriate treatment concentration of mullein，the experiment was divided into control group，H2O2（100 μmol/L）model group，H2O2 （100 μmol/L）+ Calycosin（20 μmol/L）intervention group；CCK8 method was used to detect the effect on the proliferation of astrocytes；Flow cytometry was used to detect astrocyte apoptosis；immunofluorescence was used to detect the level of Brdu in each group of cell samples；Western blot was used to detect the protein expression of p⁃AKT，GP130 and IL⁃6 in each group of cells. Results Compared with the control group，the proliferation activity of astrocytes in the H2O2 group was decreased，the degree of apoptosis was aggravated，and the protein expressions of p⁃AKT，GP130 and IL⁃6 were significantly increased（P < 0.05）. After treatment，the proliferation activity of astrocytes was significantly increased，and the apoptosis was effectively inhibited，and the protein expressions of p⁃AKT，GP130 and IL⁃6 were down⁃regulated（P < 0.05）. Conclusion Calycosin could promote the proliferation of H2O2 ⁃ induced oxidatively damaged astrocytes and inhibit their apoptosis by inhibiting the PI3K/Akt signaling pathway.