Ameliorative effect of lotus seedpod proanthocyanidins on cognitive impairment and brain aging induced by d-galactose

• Lotus seedpod proanthocyanidins (LSPC) improves cognitive deficits induced by D-galactose.
• LSPC alleviates oxidative stress and blocks Aβ1–42 overproduction in aging mice brain induced by D-galactose.
• LSPC rejuvenates acetylcholine and monoaminergic system of senescent mice induced by D-galactose.
• LSPC prevents P53 protein from expressing and neuron from apoptosis in the hippocampus of D-galactose-treated mice.
• Anti-aging has the potential to treat Alzheimer's disease.

This study mainly investigated the ameliorative effect of lotus seedpod proanthocyanidins (LSPC) and the mechanism underlying such effect on cognitive impairment and brain aging induced by d-galactose. Aging mice induced by d-galactose (150 mg/kg, sc injection daily for 6 weeks) were chosen for the experiment. LSPCs (30, 60, and 90 mg/kg, ig) were provided after d-galactose injection. Learning and memory functions were detected by Y-maze and step-down avoidance tests. Then, some biochemical indexes related to cognitive ability and aging were measured. Histopathological feature and P53 protein expression in the hippocampus were observed. Results showed that the three different doses of LSPC could significantly ameliorate the learning and memory abilities impaired by d-galactose. LSPC significantly reduced the levels of malondialdehyde and nitric oxide (i.e. 90 mg/kg LSPC group vs. model group, P = 0.008), reduced the content of β-amyloid peptide 1–42 (i.e. 90 mg/kg LSPC group vs. model group, P = 0.009), decreased the activities of acetylcholinesterase, monoamine oxidase B, total nitric oxide synthase (i.e. 90 mg/kg LSPC group vs. model group, P = 0.006), and neuronal nitric oxide synthase and synchronously increased the activities of superoxide dismutase and glutathione peroxidase in the brain. Furthermore, LSPC could prevent neuron damage and could lessen the expression of P53 protein in the hippocampus. These findings demonstrated that LSPC effectively attenuated cognitive damage and improved parameters related to brain aging in senescent mice induced by d-galactose, and may be used to treat Alzheimer's disease.