Albiflorin ameliorates memory deficits in APP/PS1 transgenic mice via ameliorating mitochondrial dysfunction

Albiflorin, the main component of Radix Paeoniae Alba, has been shown to ameliorate injury in cell models of Alzheimer's disease induced by amyloid-beta (A beta), 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 A beta 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 Drpl, increased the levels of Mfn1, Mfn2 and Opal 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 A beta deposition in the brain and ameliorated memory deficits in APP/PS1 mice. These findings indicate that albiflorin may serve as a potential antidementia drug.