Green Tea Seed Oil Suppressed Aβ1–42-Induced Behavioral and Cognitive Deficit via the Aβ-Related Akt Pathway

• Published in: International journal of molecular sciences Vol. 20; no. 8; p. 1865
• Main Authors: Kim, Jong Min, Park, Seon Kyeong, Kang, Jin Yong, Park, Su Bin, Yoo, Seul Ki, Han, Hye Ju, Cho, Kyoung Hwan, Kim, Jong Cheol, Heo, Ho Jin
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 15.04.2019; MDPI
• Subjects: AKT protein; amyloid β; Anti-inflammatory agents; Antioxidants; Aβ-related Akt pathway; Brain; Dietary fiber; Disease; Functional foods & nutraceuticals; Green tea; green tea seed oil; Inflammation; Ionic mobility; Liquid chromatography; Long term memory; Mass spectrometry; Mass spectroscopy; Memory; neuroprotective effect; Oilseeds; Oxidative stress; Peptides; Pheochromocytoma cells; Physiology; Polyphenols; Probiotics; Proteins; Quadrupoles; Seeds; Spatial discrimination learning; Spatial memory; Spices; Tea; Vitamins
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms20081865

The aim of this study was to investigate the availability of seeds, one of the byproducts of green tea, and evaluate the physiological activity of seed oil. The ameliorating effect of green tea seed oil (GTO) was evaluated on H2O2-induced PC12 cells and amyloid beta (Aβ)1–42-induced ICR mice. GTO showed improvement of cell viability and reduced reactive oxygen species (ROS) production in H2O2-induced PC12 cells by conducting the 2′,3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and 2′,7′-dichlorofluorescein diacetate (DCF-DA) analysis. Also, administration of GTO (50 and 100 mg/kg body weight) presented protective effects on behavioral and memory dysfunction by conducting Y-maze, passive avoidance, and Morris water maze tests in Aβ-induced ICR mice. GTO protected the antioxidant system by reducing malondialdehyde (MDA) levels, and by increasing superoxide dismutase (SOD) and reducing glutathione (GSH) contents. It significantly regulated the cholinergic system of acetylcholine (ACh) contents, acetylcholinesterase (AChE) activities, and AChE expression. Also, mitochondrial function was improved through the reduced production of ROS and damage of mitochondrial membrane potential (MMP) by regulating the Aβ-related c-Jun N-terminal kinase (JNK)/protein kinase B (Akt) and Akt/apoptosis pathways. This study suggested that GTO may have an ameliorating effect on cognitive dysfunction and neurotoxicity through various physiological activities.