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Objective Angelica  ( A. )  sinensis  is used as a traditional medical herb for the treatment of neurodegeneration, aging, and inflammation in Asia.  A. sinensis  optimal formula (AOF) is the best combination in  A. sinensis  that has been screened to rescue the cognitive ability in β-amyloid peptide (Aβ 25–35 )-treated Alzheimer’s disease (AD) rats. The objective of this study was to investigate the effect of AOF on the learning and memory of AD rats as well as to explore the underlying mechanisms. Methods Male Wistar rats were infused with Aβ 25–35  for AD model induction or saline (negative control). Five groups of AD rats were fed on AOF at 20, 40, or 80 mL/kg every day, donepezil at 0.9 mg/kg every day (positive control), or an equal volume of water (AD model) intragastrically once a day for 4 weeks, while the negative control rats were fed on water. The Morris water maze test was used to evaluate the cognitive function of the rats. The Aβ accumulation, cholinergic levels, and antioxidative ability were detected by ELISA. Additionally, the candidate mechanism was determined by gene sequencing and quantitative real-time polymerase chain reaction. Results The results showed that AOF administration significantly ameliorated Aβ 25–35 -induced memory impairment. AOF decreased the levels of amyloid-β precursor protein and Aβ in the hippocampus, rescued the cholinergic levels, increased the activity of superoxide dismutase, and decreased the malondialdehyde level. In addition, AOF inhibited the expression of  IL1b ,  Mpo , and  Prkcg  in the hippocampus. Conclusion These experimental findings illustrate that AOF prevents the decrease in cognitive function and Aβ deposits in Aβ 25–35 -treated rats via modulating neuroinflammation and oxidative stress, thus highlighting a potential therapeutic avenue to promote the co-administration of formulas that act on different nodes to maximize beneficial effects and minimize negative side effects.

Optimal Formula of Angelica sinensis Ameliorates Memory Deficits in β-amyloid Protein-induced Alzheimer’s Disease Rat Model