The total triterpenoid saponins of Xanthoceras sorbifolia improve learning and memory impairments through against oxidative stress and synaptic damage

Abstract

BackgroundX. sorbifolia is a widely cultivated ecologicalcrop in the north of China which is used to produce biodiesel fuel. It also possesses special medicinal value and has attracted keen interests of researchers to explore its bioactivity. PurposeTo extract the total triterpenoid saponins from the husk of X. sorbifolia (TSX) and investigate its effects on Alzheimer's disease (AD). Study designTSX was prepared via modern extraction techniques. Its effects on two AD animal models, as well as the preliminary mechanism were investigated comprehensively. MethodsThe behavioral experiments including Y maze test, Morris water maze test and passive avoidance test were performed to observe the learning and memory abilities of the animals. ELISA assays, transmission electron microscope observation and Western blotting were employed in mechanism study. ResultsTSX, the main composition of X. sorbifolia, accounted for 88.77% in the plant material. It could significantly increase the spontaneous alternation in Y maze test (F (6, 65)=3.209, P<0.01), prolong the swimming time in the fourth quadrant in probe test of Morris water maze test (F (6, 71)=4.019, P<0.01), and increase the escape latency in passive avoidance test (F (6, 65)=3.684, P<0.01) in AD model animals. The preliminary mechanism research revealed that TSX could significantly increase the contents of hippocampal Ach and ChAT, and enhance activity of ChAT in hippocampus of quinolinic acid injected rats (F (5, 61)=3.915, P 0.01; F (5, 61)=3.623, P<0.01, F (5, 61)=4.344, P<0.01, respectively). It could also increase the activities of T-AOC and T-SOD, and decrease the content of MDA in hippocampus of Aβ1-42 injected mice (F (5, 30)=5.193, P<0.01, F (5, 30)=2.865, P<0.05, F (5, 30)=4.735, P<0.01, respectively). Moreover, it significantly increased the expressions of SYP, PSD-95 and GAP-43 in hippocampus (F (4, 27)=3.495, P<0.05; F (4, 27)=2.965, P<0.05; F (4, 27)=4.365, P<0.01, respectively), and improved the synaptic ultra-structure damage in model rats. ConclusionTSX could significantly improve the impairments of learning and memory. The preliminary mechanism might associate with its protection effects against oxidative stress damage, cholinergic system deficiency and synaptic damage. TSX are perfectly suitable for AD patients as medicine or functional food, which would be a new candidate to treat AD.