Acer truncatum seed oil and Rosa roxburghii juice submicron emulsion: preparation and its therapeutic potential in alleviating scopolamine-induced memory impairment in mice

This study aimed to develop a submicron emulsion (SE) of Acer truncatum seed oil (ASO) and Rose roxburghii Tratt juice (RRTJ) using a response surface method for optimal formula screening and process parameters. The stability of ASO-RRTJ/SE and its effects on scopolamine-induced memory impairment in mice were investigated. The ASO-RRTJ/SE exhibited a desirable particle size ((276.86 ± 4.61) nm), polydispersity index (PDI, 0.22 ± 0.02), centrifugal stability parameter (Ke, 0.143 ± 0.004), and Zeta potential ((30.57 ± 2.38) mV). Morris water maze test, measurement of acetylcholine (ACh) concentration and acetylcholinesterase (AChE) activity in the hippocampus, superoxide dismutase (SOD) activity and malondialdehyde (MDA) concentration in serum, hematoxylin and eosin (H&E) staining, immunofluorescence staining were adopt to evaluate ASO-RRTJ/SE therapeutic potential in alleviating scopolamine-induced memory impairment in mice. Behavioral tests demonstrated that ASO-RRTJ/SE significantly ameliorated scopolamine-induced spatial learning and memory deficits in mice, suggesting potential neuroprotective effects against scopolamine-mediated central nervous system excitation. Compared to the Model group, the high-dose ASO-RRTJ/SE (H-SE) group displayed a 77.84% increase in hippocampal ACh content, a 46.97% decrease in AChE activity, a 29.48% increase in serum SOD activity, and a 40.15% decrease in MDA content. H&E staining of hippocampal sections revealed that the H-SE group exhibited well-organized hippocampal neurons, with a significantly reversal of nuclear pyknosis, deep staining, and cytoplasmic dissolution. The pyramidal cell layer displayed improved organization, and the intercellular distance returned to normal. Additionally, H-SE treatment significantly reduced the aggregation of phosphorylated tau protein, increased choline acetyltransferase expression, and promoted brain-derived neurotrophic factor production. In conclusion, ASO-RRTJ/SE ameliorates scopolamine-induced memory impairment in mice.