The flavonoid apigenin protects brain neurovascular coupling against amyloid-β₂₅₋₃₅-induced toxicity in mice.

摘要: Apigenin, one of the most common flavonoids, has demonstrated anti-inflammatory, anticarcinogenic, and free radical-scavenging activities. Recent studies revealed its protective effects against amyloid-β (Aβ)-induced neurotoxicity, but mechanism was unclear. In present study, we aimed to explore anti-amnesic apigenin Aβ₂₅₋₃₅-induced toxicity underlying mechanisms in cerebral cortex mice. The learning memory impairments, changes morphology major components neurovascular unit, ultrastructural oxidative stress cortex, cerebrovascular dysfunction, neuronal were detected after oral administration continuously for 8 days. Our results demonstrate that amnesic mice conferred robust coupling protection, involving improvement capabilities, maintenance unit integrity, modulation microvascular function, reduction damage, increase regional blood flow, cholinergic system inhibition AChE activity elevation ACh level, modification BNDF, TrkB, phospho-CREB levels.