人参皂苷Rg1对寡聚肽Aβ_(1-42)增加JNK活性及诱导凋亡的影响

Effect of ginsenoside Rg1 on JNK and oligomeric Aβ_(1-42)-induced apoptosis

目的：在寡聚肽Aβ1-42诱导的神经元凋亡过程中,探讨人参皂苷Rg1的保护作用和可能机制；方法运用寡聚肽Aβ1-42来诱导原代培养的皮层神经元损害,把神经元分为空白对照组、Aβ组、sp600125与Aβ共同孵育组以及人参皂苷Rg1与 Aβ共同孵育组,然后观察 JNK、p-JNK、caspase-3活性和TUNEL细胞数的变化。结果寡聚肽 Aβ1-42作用15 min,皮层神经元的JNK磷酸化水平明显增加；经过预先孵育24 h人参皂苷Rg1（2．5～10μmol·L^-1）后,再与寡聚肽Aβ1-42共同孵育15 min,JNK磷酸化水平明显降低；寡聚肽Aβ1-42孵育24 h,caspase-3活性和TUNEL数明显升高；人参皂苷Rg1（10μmol·L^-1）预处理24 h后,再与Aβ1-42共孵育24 h组中caspase-3和TUNEL阳性数目明显下降。结论人参皂苷Rg1可通过JNK通路减轻寡聚肽Aβ1-42诱导的神经元凋亡。

Aim To explore the possible protective effect of ginsenoside Rg1 on oligomeric Aβ1-42 induced apoptosis and its possible mechanism. Methods The damage was induced by oligomeric Aβ1-42 in primary cortical neurons. Cells were incubated in the absence or presence of Aβ, or co-incubated in sp600125 with Aβ, or pre-incubated in ginsenoside Rg1 then co-incu-bated in Aβ. The p-JNK, JNK, caspase-3 activity and TUNEL-positive cells were detected. Results In Aβ1-42 treated group, the ratio of p-JNK/JNK level was increased more than that in non-treated group for 15min. However, in neurons preincubated with （2. 5, 5, 10 μmol·L^-1 ） ginsenoside Rg1 and then co-incuba-ted with 5 μmol·L^-1 oligomeric Aβ1-42 , the p-JNK/JNK ratio, caspase-3 activity and TUNEL positive neu-rons were significantly decreased compared with those of Aβ1-42 treated group. Conclusion Ginsenoside Rg1 can attenuate the oligomeric Aβ1-42-induced apop-tosis by JNK pathway.