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

Autor: Zhi-Da Sun, Yu-Shi Gong, Bijun Xie, Fang-Li Hou, Kun Hu, Yong-Qing Gao, Juan Guo, Er-Ning Yang
Rok vydání: 2015
Předmět:
0301 basic medicine
Male
Aging
Time Factors
Biochemistry
Hippocampus
chemistry.chemical_compound
Mice
0302 clinical medicine
Endocrinology
Cognition
Hippocampus (mythology)
chemistry.chemical_classification
Neurons
biology
Behavior
Animal
Glutathione peroxidase
Age Factors
Malondialdehyde
Acetylcholinesterase
Nitric oxide synthase
Neuroprotective Agents
Seeds
Female
Monoamine oxidase B
medicine.medical_specialty
Nitric oxide
Superoxide dismutase
03 medical and health sciences
Memory
Internal medicine
Genetics
medicine
Avoidance Learning
Animals
Proanthocyanidins
Maze Learning
Molecular Biology
Plants
Medicinal
Dose-Response Relationship
Drug
Plant Extracts
Galactose
Cell Biology
Disease Models
Animal
030104 developmental biology
chemistry
biology.protein
Lotus
Cognition Disorders
030217 neurology & neurosurgery
Biomarkers
Phytotherapy
Zdroj: Experimental gerontology. 74
ISSN: 1873-6815
Popis: 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.
Databáze: OpenAIRE
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