akebia-saponin-d and Memory-Disorders

Glucocorticoid hormones are implicated in the pathogenesis of Alzheimer's disease (AD) and other diseases including diabetes, hyperlipidemia, and osteoporosis. Akebia saponin D (ASD) possesses numerous pharmacological activities, including as an anti-AD, anti-hyperlipidemia, anti-diabetes, and anti-osteoporosis agent. The anti-AD effect of ASD is possibly through its regulation of glucocorticoid levels.. The present study was undertaken to investigate the neuroprotective effects of ASD on Aβ. The AD rat model was established by an intracerebroventricular injection of Aβ. Compared with the control group, AD rats displayed significant spatial learning and reference memory impairments, serious anxiety disorders, obvious hypertrophy of adrenal gland, elevated corticosterone and ACTH levels in the plasma, and increased 11β-HSD1 activity in liver and groin fat pad. ASD could significantly ameliorate the memory deficits and anxiety symptoms, markedly reduce the viscera coefficient of adrenal gland, observably decrease corticosterone and ACTH concentrations, and showed no effect on the activity of 11β-HSD1.. These results indicate that ASD might exert a significant neuroprotective effect on cognitive impairment, driven in part by reducing systemic corticosterone level by down-regulation of the hypothalamic-pituitary-adrenal (HPA) axis.

Topics: 11-beta-Hydroxysteroid Dehydrogenase Type 1; Adipose Tissue; Adrenal Glands; Alzheimer Disease; Amyloid beta-Peptides; Animals; Anxiety; Corticosterone; Disease Models, Animal; Hypertrophy; Hypothalamo-Hypophyseal System; Liver; Male; Maze Learning; Memory Disorders; Models, Biological; Peptide Fragments; Pituitary-Adrenal System; Rats, Sprague-Dawley; Saponins; Viscera