Ecklonia cava Ameliorates Cognitive Impairment on Amyloid β-Induced Neurotoxicity by Modulating Oxidative Stress and Synaptic Function in Institute of Cancer Research (ICR) Mice

• Published in: Antioxidants Vol. 13; no. 8; p. 951
• Main Authors: Lee, Hyo Lim, Go, Min Ji, Lee, Han Su, Heo, Ho Jin
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 06.08.2024; MDPI
• Subjects: Acids; Alzheimer's disease; antioxidants; Apoptosis; Behavior; Bioactive compounds; Biochemical analysis; Brain research; Brain-derived neurotrophic factor; c-Jun protein; Care and treatment; Cerebral cortex; Chemical properties; cholinergic system; Chromatography; Cognition disorders; Cognitive ability; dieckol; Dietary supplements; Ecklonia cava; Ethanol; Glutathione; Health aspects; High-performance liquid chromatography; JNK protein; Marine algae; marine polyphenol; Mass spectroscopy; Medical research; Membrane potential; Memory; Neurodegenerative diseases; neuroinflammation; Neuropharmacology; Neuroprotection; Neurotoxic agents; Neurotoxicity; NF-κB protein; Oxidative stress; Peptides; Physiological aspects; Physiology; Polyphenols; Reactive oxygen species; Structural proteins; Superoxide dismutase; Synapses; Transcription factors; Water; β-Amyloid; South Korea; United States > US; Germany; Alzheimer’s disease; antioxidants; neuroinflammation; cholinergic system; Ecklonia cava; dieckol; marine polyphenol
• ISSN: 2076-3921; 2076-3921
• DOI: 10.3390/antiox13080951

This study investigated the neuroprotective effect of 70% ethanol extract of (EE) in amyloid beta (Aβ)-induced cognitive deficit mice. As a result of analyzing the bioactive compounds in EE, nine compounds were identified using ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS). In particular, the diekcol content was quantified by high-performance liquid chromatography with diode-array detection (DAD-HPLC). Biochemical analysis was performed on brain tissue to determine the mechanism of the cognitive function improvement effect of EE. The result showed that EE ameliorated learning and memory decline in behavioral tests on Aβ-induced mice. EE also attenuated oxidative stress by regulating malondialdehyde (MDA) content, reduced glutathione (GSH), and superoxide dismutase (SOD) levels. Similarly, EE also improved mitochondrial dysfunction as mitochondrial membrane potential, ATP production, and reactive oxygen species (ROS) levels. In addition, EE enhanced synapse function by modulating acetylcholine-related enzymes and synaptic structural proteins in the whole brain, hippocampus, and cerebral cortex tissues. Also, EE regulated Aβ-induced apoptosis and inflammation through the c-Jun N-terminal kinase (JNK) and nuclear factor-kappa B (NF-κB) signaling pathways. Furthermore, EE protected neurotoxicity by increasing brain-derived neurotrophic factor (BDNF) production. These results suggest that EE may be used as a dietary supplement for the prevention and treatment of Alzheimer's disease (AD).