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目的:探讨西洋参皂苷(PQLS)抑制缺氧诱导的胚鼠大脑皮层神经细胞凋亡的作用机理。方法:正常对照组、凋亡阳性组、西洋参皂苷0.025g/L组、0.05g/L组、0.1g/L组、0.2g/L组;SD胚大鼠原代大脑皮层神经细胞体外无血清缺氧-复氧培养;应用MTT、DNA电泳、免疫细胞化学染色等方法观察西洋参皂苷的适宜剂量、DNA凋亡条带及凋亡调节蛋白Bcl-2、Bax、Caspase-3的表达率。结果:①缺氧条件下PQLS在0.05～0.1g/L促进缺氧的神经细胞增殖较凋亡阳性组提高31.17%～37.65%(P﹤0.01)。②0.05～0.2g/L的PQLS使缺氧的神经细胞DNA只出现3条凋亡条带(凋亡阳性组6条带),且条带浓度也明显降低。③0.025g/L～0.1g/L PQLS显著减少缺氧的神经细胞表达Bax(67.02±1.69%～57.97±2.6%,凋亡阳性组72.19±3.97%,P<0.05～0.01)和Caspase-3(62.27±2.02%～50.34±2.65%,凋亡阳性组68.62±1.40%,P<0.05～0.01);提高缺氧的神经细胞表达Bcl-2(44.22±3.73%～63.76±2.96%,凋亡阳性组35.61±2.16%,P<0.01)和Bcl-2/Bax比值(0.69±0.11～1.11±0.04,凋亡阳性组0.56±0.11,P<0.05～0.01)。结论:西洋参皂苷通过降低缺氧的神经细胞表达Bax、Caspase-3,提高Bcl-2的表达及Bcl-2/Bax比例阻断缺氧诱导的神经细胞凋亡,保护缺氧的神经细胞。
Objective: To investigate the mechanism of action of Panax Notoginseng Saponins (PQLS) on neuronal apoptosis induced by hypoxia in cerebral cortex of embryo. Methods: The normal control group, apoptotic group, ginsenoside 0.025g / L group, 0.05g / L group, 0.1g / L group, 0.2g / L group; SD rat embryonic rat primary cerebral cortex neurons in vitro serum Hypoxia-reoxygenation culture. Appropriate dose of ginsenoside, apoptotic bands of DNA and the expressions of Bcl-2, Bax and Caspase-3 were observed by MTT, DNA electrophoresis and immunocytochemical staining. Results: ① Under hypoxia, PQLS promoted the hypoxia-induced neuronal proliferation by 31.17% -37.65% (P <0.01) in the group of apoptotic positive cells at 0.05 ~ 0.1g / L. ② PQLS of 0.05 ~ 0.2g / L showed only 3 apoptotic bands in hypoxic neuronal DNA (6 bands of apoptotic positive group), and the band concentration was significantly decreased. P0.025g / L ~ 0.1g / L PQLS significantly reduced the expression of Bax (67.02 ± 1.69% -57.97 ± 2.6%, apoptotic positive group 72.19 ± 3.97%, P <0.05 ~ 0.01) and Caspase-3 (62.27 ± 2.02% -50.34 ± 2.65%), apoptotic positive group (68.62 ± 1.40%, P <0.05-0.01), and increased the expression of Bcl-2 in hypoxic neurons (44.22 ± 3.73% -63.76 ± 2.96% (35.61 ± 2.16%, P <0.01) and Bcl-2 / Bax ratio (0.69 ± 0.11 ~ 1.11 ± 0.04, 0.56 ± 0.11, P <0.05 ~ 0.01) CONCLUSION: Ginsenoside can protect hypoxic neurons by reducing the expression of Bax and Caspase-3 in hypoxic neurons, increasing the expression of Bcl-2 and the ratio of Bcl-2 / Bax in hypoxia-induced neuronal apoptosis.