Albiflorin, the main component of Radix Paeoniae Alba, has been shown to ameliorate injury in cell models of
Alzheimer's disease induced by
amyloid-β (Aβ), but the mechanism is unclear. We used 7-month-old APP/PS1 mice to determine whether
albiflorin is capable of protecting against
Alzheimer's disease. We found that four weeks of intragastric administration of
albiflorin (20 mg/kg/d and 40 mg/kg/d) ameliorated
memory deficits in APP/PS1 mice.
Albiflorin conferred synaptic protection by decreasing Aβ levels and increasing PSD-95,
synaptophysin and
synapsin 1 levels in the brains of APP/PS1 mice.
Albiflorin played an antioxidative role by reducing
reactive oxygen species (ROS) levels and elevating
Mn-SOD activity in the brain.
Albiflorin also reduced the level of Drp1, increased the levels of Mfn1, Mfn2 and Opa1 and improved mitochondrial morphology in APP/PS1 mice.
Albiflorin inhibited the mitochondrial pathway of apoptosis by increasing the levels of Bcl-2 and Bcl-xl and decreasing the levels of Bax,
caspase-3 and
cytochrome c in both the hippocampus and the cortex and by reducing the number of apoptotic cells in the anterior parietal cortex of the APP/PS1 mice. In conclusion, treatment with
albiflorin improved mitochondrial function, reduced Aβ deposition in the brain and ameliorated
memory deficits in APP/PS1 mice. These findings indicate that
albiflorin may serve as a potential antidementia
drug.