Hydroalcoholic extract from Abelmoschus manihot (Linn.) Medicus flower reverses sleep deprivation-evoked learning and memory deficit. Issue 10 (1st October 2020)

• Record Type: Journal Article
• Authors: Zhou, Hai-rui; Wu, Jing-ru; Bei, Lei; Wang, Bai-xin; Xu, Hui; Wang, Jing-tao; Ma, Shu-xia
• Is Part Of: Food & function. Volume 11:Issue 10(2020)
• Page Start: 8978
• Page End: 8986
• Publication Date: 2020-10-01
• Subjects: Food -- Analysis -- Periodicals; Food -- Composition -- Periodicals; Nutrition -- Periodicals; 664.07
• DOI: 10.1039/d0fo02158j
• Languages: English
• ISSNs: 2042-6496

Abstract

Abstract : Extract of Abelmoschus manihot flower (EAM) has the potential to ameliorate learning and memory deficit, in part through inhibiting oxidative stress in the brain. Abstract : Previous researches have indicated that sleep plays a vital role in cognitive functions. Sleep deprivation (SD) causes learning and memory damage, which is associated with oxidative stress. This study was performed to investigate the neuroprotective effects of an extract of Abelmoschus manihot flower (EAM) against memory deficit induced by SD in mice. The SD model was evoked by multiple platform method for 5 days, successively. The learning and memory-improving effects of EAM were assessed by behavioral trials and the underlying mechanism was investigated by measuring the oxidative stress alteration. Our findings indicated that the SD-induced memory deficit and the EAM treatment improved the cognitive functions of mice in the object location recognition test and passive avoidance task. In addition, EAM effectively improved the activities of the antioxidant enzyme, decreased the content of malondialdehyde (MDA), and restored the protein expression of the brain-derived neurotrophic factor (BDNF), tyrosine kinase B (TrkB) and glutamate receptor 1 (GluR1) in brain tissues. In conclusion, EAM could improve the SD-evoked learning and memory impairments. The possible underlying mechanisms of EAM may be related to its antioxidant capacity and enhanced BDNF/TrkB/GluR1 levels in the hippocampal memory.