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目的探讨人参皂甙Rb1对体外培养的新生大鼠大脑皮层神经细胞缺氧性凋亡的保护机理。方法应用“Neurobasal加B2 7Supplement”体外培养大鼠大脑皮层神经细胞 ,并在缺氧条件下使用台盼蓝拒染法、Hoechst 3 3 3 42荧光染色法、免疫细胞化学染色法观察人参皂甙Rb1对原代神经细胞的抗凋亡保护作用。结果在 10— 10 0 μg/ml的浓度范围内 ,人参皂甙Rb1能降低缺氧诱导的神经细胞凋亡率 (10 0 μg/ml组 ,P <0 .0 5 ) ,增加缺氧神经细胞Bcl 2蛋白的表达 (5 0— 10 0 μg/ml组 ,P <0 .0 5 ) ,同时减少Bax蛋白的表达 (5 0— 10 0 μg/ml组 ,P <0 .0 5—P <0 .0 0 1) ,提高Bcl 2 /Bax比值 (5 0— 10 0 μg/ml组 ,P <0 .0 5 )。 结论在 5 0— 10 0μg/ml的浓度范围内 ,人参皂甙Rb1通过上调缺氧神经细胞Bcl 2表达和下调Bax表达 ,避免缺氧神经细胞凋亡。
Objective To investigate the protective mechanism of ginsenoside Rb1 on apoptosis of neonatal rat cerebral cortical neurons in vitro. Methods Rat cerebral cortical neurons were cultured in vitro using Neurobasal plus B2 7 Supplement. Trypan blue staining, Hoechst 3 3 42 fluorescence staining, and immunocytochemistry were used to observe the effect of ginsenoside Rb1 on hypoxic conditions. Primary anti-apoptosis protection of nerve cells. Results In the concentration range of 10-10 μg/ml, ginsenoside Rb1 could decrease the apoptosis rate of neurons induced by hypoxia (10 μg/ml group, P <0.05) and increase the number of hypoxic neurons Bcl. 2 protein expression (50-100 μg/ml group, P < 0.05), while reducing the expression of Bax protein (50-100 μg/ml group, P <0.05-P <0 .0 0 1) , increase the Bcl 2 /Bax ratio (50-100 μg/ml group, P <0.05). Conclusion In the concentration range of 50-10.0μg/ml, ginsenoside Rb1 up-regulates the expression of Bcl 2 and down-regulates Bax expression in hypoxic neurons and avoids apoptosis of hypoxic neurons.