orientin and Cognition-Disorders

There is increasing evidence that chronic noise stress impairs cognition and induces oxidative stress in the brain. Recently, orientin, a phenolic compound abundant in some fruits, millet, and herbs, has been shown to have antioxidant properties. This study investigated the potential effects of orientin against chronic noise-induced cognitive decline and its underlying mechanisms. A moderate-intensity noise exposure model was used to investigate the effects of orientin on behavior and biochemical alterations in mice. After 3 weeks of the noise exposure, the mice were treated with orientin (20mg/kg and 40 mg/kg, oral gavage) for 3 weeks. The chronic noise exposure impaired the learning and memory in mice in the Morris water maze and step-through tests. The noise exposure also decreased exploration and interest in a novel environment in the open field test. The administration of orientin significantly reversed noise-induced alterations in these behavior tests. Moreover, the orientin treatment significantly improved the noise-induced alteration of serum corticosterone and catecholamine levels and oxidative stress in the hippocampus and prefrontal cortex. Furthermore, the orientin treatment ameliorated the noise-induced decrease in brain-derived neurotrophic factor and synapse-associated proteins (synaptophysin and postsynaptic density protein 95) in the hippocampus and prefrontal cortex. Thus, orientin exerts protective effects on noise-induced cognitive decline in mice, specifically by improving central oxidative stress, neurotransmission, and increases synapse-associated proteins. Therefore, supplementation with orientin-enriched food or fruit could be beneficial as a preventive strategy for chronic noise-induced cognitive decline.

Topics: Animals; Behavior, Animal; Cognition Disorders; Flavonoids; Glucosides; Hippocampus; Male; Mice; Neuronal Plasticity; Noise; Oxidative Stress; Prefrontal Cortex; Synaptic Transmission

β-Amyloid (Aβ)-mediated neurotoxicity plays a critical role in the pathogenesis of Alzheimer's disease (AD), possibly including Aβ-induced mitochondrial dysfunction and oxidative stress. Previous studies have demonstrated that orientin (Ori) possesses antioxidation capabilities in vitro. Therefore, current study is to demonstrate that Ori can activate Nrf2/HO-1 signaling and alleviate apoptosis induced by Aβ1-42, and ameliorate cognitive deficits in AD mice.. AD models were made by injecting Aβ1-42 into the bilateral hippocampus of mice. The mice were randomly assigned to three groups: the normal mice and Aβ1-42-induced AD mice with saline, and Aβ1-42-induced AD mice with Ori (5mg/kg), and were injected intraperitoneally once a day for 15 days. After the Morris Water Maze (MWM) test, mice were sacrificed and brains were harvested for biochemical analysis.. Results indicated that Ori could ameliorate cognitive deficits in AD mice. Levels of oxidative stress, indicated by production of reactive oxygen species (ROS), 3-nitrotyrosine (3-NT), 4-hydroxy-nonenal (4-HNE) and 8-hydroxy-2'-deoxyguanosine (8-OHdG), were significantly decreased after Ori treatment. In addition, the current study showed that Ori could attenuate mitochondrial dysfunction induced by Aβ1-42, and subsequently inhibited the mitochondrial apoptotic pathway. Ori induced the nuclear translocation of Nrf2, which enhanced the expression of HO-1 and activation of the redox signaling pathway.. Ori might alleviate cognitive deficits and oxidative stress in AD mice, which might be a potential therapeutic drug for AD.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Apoptosis; Cognition Disorders; Flavonoids; Free Radical Scavengers; Glucosides; Heme Oxygenase-1; Male; Maze Learning; Membrane Potential, Mitochondrial; Mice; Mice, Inbred C57BL; NF-E2-Related Factor 2; Oxidative Stress; Peptide Fragments; Reactive Oxygen Species; Signal Transduction