Neuroprotective effects of Bouea macrophylla leaf extract against amyloid-beta peptide-induced toxicity in human neuroblastoma SH-SY5Y cells

Purpose: Alzheimer's disease (AD) is the most common type of dementia, which is thought to be caused by the abnormal buildup of proteins including amyloid-beta (A) in and around brain cells. In efforts to discover new strategies for AD therapy, natural products have aroused interest in the research community and in the pharmaceutical industry for their neuroprotective activity, targeting different pathological mechanisms associated with AD. A wide variety of natural products from different origins have been evaluated preclinically and clinically for their neuroprotective mechanisms in preventing and attenuating the multifactorial pathologies of AD. Our initial previous study demonstrated the chemical constituents from the leaves of the Bouea macrophylla Griff (B. macrophylla) could serve as source of bioactive compounds with potential antimicrobial, antioxidant and anticancer properties. However, their neuroprotective effects on A-induced cytotoxicity has not been described yet. Methods: In our continuing search for bioactive from the leaves of B. macrophylla, we herein describe its cytotoxicity against a neuroblastoma cell line (SH-SY5Y) anti-A aggregation potential, and neuroprotective potential. Results: Thioflavin T assay revealed that the inhibition potential of ethanolic extract was 60.65% at 50 μg/mL compared to the positive control group (p < 0.05), while neuroprotective effects were elaborated against Aβ-induced SH-SY5Y cells at 25 μg/mL. In order to validate these neuroprotective effects, the ethanol extract revealed reductions in the intracellular ROS (reactive oxygen species) level in H2O2-treated SH-SY5Y cells and mitochondrial dysfunctions in Aβ-induced SH-SY5Y cells at 25 μg/mL. Consclusions: The overall results have provided scientific insights of utilizing B. macrophylla as a potential anti-Aβ and neuroprotection agent containing secondary metabolites which may be pharmacologically relevant.