Effect of ginsenoside Rg1 on oligomeric Aβ (1-42) inhibition of PKA/CREB pathway

Objective To investigate the possible effect of ginsenoside Rg1 and oligo Aβ1-42 on PKA/CREB pathway. Methods The damage was induced by oligomeric Aβ1-42 in primary cortical neuron. Neurons were incubated with or without glutamate, or incubated in Aβ, or pre-incubated in Rg1 and then co-incubated in Aβ. The proteins of p-CREB, t-CREB, PKAⅡα and BDNF were detected by Western blot. Results After the treatment with Oligo Aβ1-42 for 2 h, the p-CREB/t-CREB level induced by glutamate was obviously lower (P<0.001). However, in neurons pre-incubated with 2.5, 5.0, 10.0 μmol/L of ginsenoside Rg1 and then co-incubated with 5 μmol/L of oligo Aβ1-42, the p-CREB/ t-CREB induced by glutamate was significantly increased as compared with that of Aβ1-42 group (P<0.05). Upon Aβ1-42 exposure for 2 h, cortical neurons showed a statistically significant increase in PKAⅡα as compared to the control group (P<0.001). Pre-treatment with varying doses of ginsenoside Rg1 (2.5, 5, 10 μmol/L) showed a decrease in PKAⅡα as compared to neurons treated with Aβ1-42 alone for 2 h (P<0.001). Furthermore, BDNF level significantly increased in Rg1-pretreated cells as compared to cells treated with Aβ1-42 alone for 24h (P<0.05). Conclusions Ginsenoside Rg1 attenuates the oligo Aβ1-42 inhibition of PKA/CREB pathway. Key words: Ginsenoside; Amyloid beta-protein; Protein kinases