alkaloids decrease Aβ by regulating α- and β-secretases in hippocampal neurons of SD rats.

Background: Alzheimer's disease (AD) is the primary cause of dementia in the elderly. The imbalance between production and clearance of amyloid β (Aβ) is a very early, often initiating factor in AD. Lindl. alkaloids (DNLA) extracted from a Chinese medicinal herb, which have been shown to have anti-aging effects, protected against neuronal impairment and . Moreover, we confirmed that DNLA can improve learning and memory function in elderly normal mice, indicating that DNLA has potential health benefits. However, the underlying mechanism is unclear. Therefore, we further explored the effect of DNLA on neurons, which is closely related to learning and memory, based on Aβ.

Methods: We exposed cultured hippocampal neurons to DNLA to investigate the effect of DNLA on Aβ . Cell viability was evaluated by MTT assays. Proteins were analyzed by Western blot analysis.

Results: The cell viability of hippocampal neurons was not changed significantly after treatment with DNLA. But DNLA reduced the protein expression of amyloid precursor protein (APP), disintegrin and metalloprotease 10 (ADAM10), β-site APP cleaving enzyme 1 (BACE1) and Aβ of hippocampal neurons in rats and increased the protein expression of ADAM17.

Conclusions: DNLA decreases Aβ by regulating α- and β-secretase in hippocampal neurons of SD rats.