Protective effects of ginsenoside Rg2 against memory impairment and neuronal death induced by Aβ25-35 in rats

Ethnopharmacological relevance: Ginsenoside Rg2 is an important ingredient of Panax ginseng which often appears in ancient prescriptions for forgetfulness. Ginsenoside Rg2 exert neuroprotective effects and could be a new potential medicine to treat AD. In our previous study, we reported that ginsenoside Rg2 appears protect PC12 cells against Amyloid beta-fragment (25-35) (A beta(25-35))-induced apoptosis via the PI3K/Akt pathway. However, there are no in vivo studies on the protective effects of ginsenoside Rg2 on A beta-induced neurotoxicity. Aim of the study: The present study was performed to investigate the protective effects of ginsenoside Rg2 against A beta(25-35)-induced memory impairment, and its underlying mechanisms in rats. Materials and methods: An Alzheimer's Disease (AD) rat model was established by injecting the rats with A beta(25-35) (1 mu g/mu l). Cognitive performance was evaluated by the Morris Water Maze test (MWM). The brain sections were processed and neuronal apoptosis in the hippocampus was evaluated by Hematoxylin and Eosin staining (H&E). To explore the anti-neuronal apoptosis mechanism of ginsenoside Rg2, we analyzed the protein expression of Bcl-2/Bax, caspase-3, and phospho-protein kinase B/protein kinase B (p-Akt/Akt) via western blot. Results: A significant improvement in cognitive function was observed in administrated ginsenoside Rg2 AD rats. The histological injury in hippocampus CA1 induced by A beta(25-35) was inhibited following administration of the ginsenoside Rg2. Ginsenoside Rg2 increase the Bcl-2/Bax ratio, attenuate the cleavage of caspase-3, and enhance the phosphorylation of Akt. Conclusions: These findings suggest that ginsenoside Rg2 could ameliorate A beta(25-35)-induced cognitive dysfunction by activating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway.

Automated summary

The research found that ginsenoside Rg2 can improve Aβ(25-35)-induced cognitive dysfunction by activating the PI3K/Akt signaling pathway, and inhibiting neuronal apoptosis by increasing the Bcl-2/Bax ratio, attenuating caspase-3 cleavage, and enhancing Akt phosphorylation.