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

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 sh...

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Published inInternational 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
LanguageEnglish
Published Basel MDPI AG 15.04.2019
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Abstract 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.
AbstractList 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.
Nutraceuticals include dietary fiber, probiotics, prebiotics, polyunsaturated fatty acids, antioxidant vitamins, polyphenols, and spices, which are known to have antioxidant and anti-inflammatory properties [9]. [...]tea seeds are almost always discarded after harvest because they are not used to make oil, even though they contain a variety of physiologically active substances [15]. [...]the major aim of this study concerning the evaluation of availability of green tea oil, which is one of the byproducts of green tea, was to investigate the neuronal protective effect in PC12 cells and cognitive dysfunction-induced mice. 2. Identification of Main Compounds Using UPLC Q-TOF/MS2 The major physiological compounds of green tea seed oil (GTO) were qualitatively identified using ultra-performance liquid chromatography-ion mobility separation-quadrupole time of flight/tandem mass spectrometry (UPLC IMS Q-TOF/MS2) analysis (Figure 1 and Table 1). Morris Water Maze Test To measure spatial learning acquisition and long-term memory, a Morris water maze test was performed (Figure 5).
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 H 2 O 2 -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 H 2 O 2 -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.
Author Heo
Han
Yoo
Cho
Kang
Kim
Park
AuthorAffiliation 1 Division of Applied Life Science (BK21 plus), Institute of Agriculture and Life Science, Gyeongsang National University, Jinju 52828, Korea; myrock201@naver.com (J.M.K.); tjsrud2510@naver.com (S.K.P.); kangjy2132@naver.com (J.Y.K.); tbsk5670@naver.com (S.B.P.); ysyk9412@naver.com (S.K.Y.); gksgpwn2527@naver.com (H.J.H.)
2 Institute of Hadong Green Tea, Hadong 52304, Korea; ckh8568@hgreent.or.kr (K.H.C.); jckim@hgreent.or.kr (J.C.K.)
AuthorAffiliation_xml – name: 1 Division of Applied Life Science (BK21 plus), Institute of Agriculture and Life Science, Gyeongsang National University, Jinju 52828, Korea; myrock201@naver.com (J.M.K.); tjsrud2510@naver.com (S.K.P.); kangjy2132@naver.com (J.Y.K.); tbsk5670@naver.com (S.B.P.); ysyk9412@naver.com (S.K.Y.); gksgpwn2527@naver.com (H.J.H.)
– name: 2 Institute of Hadong Green Tea, Hadong 52304, Korea; ckh8568@hgreent.or.kr (K.H.C.); jckim@hgreent.or.kr (J.C.K.)
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Snippet 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....
Nutraceuticals include dietary fiber, probiotics, prebiotics, polyunsaturated fatty acids, antioxidant vitamins, polyphenols, and spices, which are known to...
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SubjectTerms 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
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Title Green Tea Seed Oil Suppressed Aβ1–42-Induced Behavioral and Cognitive Deficit via the Aβ-Related Akt Pathway
URI https://www.proquest.com/docview/2333595884
https://search.proquest.com/docview/2210952191
https://pubmed.ncbi.nlm.nih.gov/PMC6514763
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Volume 20
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