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Vascular dementia (VD), a chronic syndrome of acquired intellectual impairment resulting from cerebrovascular diseases, is closely linked to neuronal autophagy and apoptosis. As a standardized extract from Ginkgo biloba L. leaves, EGb761 is widely applied for treating cerebrovascular diseases owing to its neuroprotective effects, with on-going research exploring its therapeutic mechanisms. Rat model of VD and SH-SY5Y cell model with OGD/R injury was applied for this study. Results showed that EGb761 reduces OGD/R-elicited apoptosis and autophagosome production, whereas improving the viability of hippocampal neurons. EGb761 treatment led to a decrease in the ratios of p-AMPK/AMPK, Bax/Bcl-2, cleaved caspase-3/caspase-3, cleaved caspase-9/caspase-9, LC3-II/LC3-I, and level of Beciln-1, as well as enhancing the proportion of p-mTOR/mTOR. Additionally, EGb761 indicated a protective effect on rats' cognitive function. These results demonstrated EGb761′s specific therapeutic mechanism in preventing apoptosis and autophagy in VD models and improving cognitive functioning in VD rats through AMPK-mTOR signalling.

Argininyl-fructosyl-glucose (AFG), a distinctive non-saponin compound isolated from red ginseng (Panax ginseng. C.A. Meyer), demonstrates neuroprotective effects. However, the molecular mechanism underlying AFG's anti-aging properties remains unclear. This study established an in vitro D-galactose-induced N2a cells subacute aging model to investigate AFG's anti-aging activity and potential mechanisms. Results indicated that AFG treatment (8 μM) significantly reduces the overexpression of aging-related proteins (p53/p21/p16) induced by D-galactose, highlighting its anti-aging efficacy. AFG concurrently diminishes ROS accumulation, lowering extracellular lactate dehydrogenase and alleviating intracellular oxidative stress. Notably, AFG suppresses the PERK/CHOP/caspase 12 pathway, reducing intracellular Ca2+ concentration and mitigating endoplasmic reticulum (ER) stress. Additionally, AFG decreases Bax and caspase 3 expression, elevates Bcl-2 and mitochondrial membrane potential, mitigating apoptosis. NAC with 4-PBA validated the results. Overall, AFG protects N2a cells from aging by reducing ER stress and apoptosis, suggesting its potential as a key substance for treating aging and neurodegenerative diseases.