Ginsenoside Rd prevents glutamate-induced apoptosis in rat cortical neurons
Ginsenoside Rd prevents glutamate-induced apoptosis in rat cortical neurons
复制标题
人参皂苷 Rd 可预防谷氨酸诱导的大鼠皮质神经元细胞凋亡
DOI：
10.1111/j.1440-1681.2009.05286.x
复制
发表时间：
2010-02-01
影响因子：
2.9
通讯作者：
Guan, Yong-Yuan
中科院分区：
文献类型：
--
作者：
Li, Xiao-Yan;Liang, Jian;Guan, Yong-Yuan
1. 电压依赖性 Ca2+ 内流在细胞凋亡中的作用最近受到了相当多的关注。已发现人参皂苷 Rd 显着抑制电压无关的 Ca2+ 进入。本研究的目的是探讨人参皂苷Rd对谷氨酸诱导的大鼠皮层神经元凋亡的保护作用。 2． Ginsenoside Rd 显着减少谷氨酸诱导的细胞凋亡形态变化和 DNA 阶梯。相比之下，尼莫地平的作用较弱。 3．人参皂苷Rd（1、3和10μmol/L）浓度依赖性地抑制caspase 3活化和活性caspase 3 p20亚基的表达（与单独谷氨酸相比，分别抑制30±10％、41±9％和62±19％；P < 0.05），而1μmol/L尼莫地平则没有影响。4．谷氨酸将细胞活力降低至 37.4 +/- 4.7 (n = 8)，并诱发细胞凋亡。人参皂苷 Rd（1、3、10 和 30 mu mol/L）浓度依赖性地抑制谷氨酸诱导的细胞死亡，增加细胞活力并降低凋亡百分比（分别从 47.5 +/- 4.9% 到 37.4 +/- 6.9%、28.3 +/- 5.2% 和 22.5 +/- 5.6%；P < 0.05）。在1μmol/L时，尼莫地平对细胞活力没有影响。此外，虽然1、3、10、30和60μmol/L人参皂苷Rd浓度依赖性地分别抑制谷氨酸诱导的Ca2+内流8+/-2%、24+/-4%、40+/-7%、49+/-8%和50+/-8%(P<0.05)，但尼莫地平没有效果。5．总之，结果表明人参皂苷Rd可防止谷氨酸诱导的大鼠皮质神经元凋亡，并进一步证明电压非依赖性Ca2+通道阻滞剂作为新型神经保护药物预防脑缺血引起的神经元凋亡和死亡的潜力。
1. The role of voltage-independent Ca2+ entry in cell apoptosis has recently received considerable attention. It has been found that ginsenoside Rd significantly inhibits voltage-independent Ca2+ entry. The aim of the present study was to investigate the protective effects of ginsenoside Rd against glutamate-induced apoptosis of rat cortical neurons.2. Ginsenoside Rd significantly reduced glutamate-induced apoptotic morphological changes and DNA laddering. In comparison, nimodipine only had a weak effect.3. Ginsenoside Rd (1, 3 and 10 mu mol/L) concentration-dependently inhibited caspase 3 activation and expression of the p20 subunit of active caspase 3 (by 30 +/- 10%, 41 +/- 9% and 62 +/- 19%, respectively, compared with glutamate alone; P < 0.05), whereas 1 mu mol/L nimodipine had no effect.4. Glutamate decreased cell viability to 37.4 +/- 4.7 (n = 8) and evoked cell apoptosis. Ginsenoside Rd (1, 3, 10 and 30 mu mol/L) concentration-dependently inhibited glutamate-induced cell death, increased cell viability and reduced apoptotic percentage (from 47.5 +/- 4.9% to 37.4 +/- 6.9%, 28.3 +/- 5.2% and 22.5 +/- 5.6%, respectively; P < 0.05). At 1 mu mol/L, nimodipine had no effect on cell viability. Furthermore, although 1, 3, 10, 30 and 60 mu mol/L ginsenoside Rd concentration-dependently inhibited glutamate-induced Ca2+ entry by 8 +/- 2%, 24 +/- 4%, 40 +/- 7%, 49 +/- 8% and 50 +/- 8% (P < 0.05), respectively, nimodipine had no effect.5. In conclusion, the results indicate that ginsenoside Rd prevents glutamate-induced apoptosis in rat cortical neurons and provide further evidence of the potential of voltage-independent Ca2+ channel blockers as new neuroprotective drugs for the prevention of neuronal apoptosis and death induced by cerebral ischaemia.