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N-3 Polyunsaturated Fatty Acids Decrease the Protein Expression of Soluble Epoxide Hydrolase via Oxidative Stress-Induced P38 Kinase in Rat Endothelial Cells
by
Okada, Takashi
, Maegawa, Hiroshi
, Imamura, Takeshi
, Morino, Katsutaro
, Kondo, Keiko
, Tawa, Masashi
, Nakagawa, Fumiyuki
, Sekine, Osamu
, Okamura, Tomio
, Ugi, Satoshi
in
Acetylcholine - pharmacology
/ acetylcysteine
/ Animal Feed - analysis
/ Animals
/ Antigens, CD
/ antioxidants
/ aorta
/ Aorta - drug effects
/ arachidonic acid
/ Cadherins
/ cardioprotective effect
/ diet
/ Dietary Supplements
/ docosahexaenoic acid
/ Docosahexaenoic Acids - chemistry
/ Docosahexaenoic Acids - pharmacology
/ eicosapentaenoic acid
/ Eicosapentaenoic Acid - chemistry
/ Eicosapentaenoic Acid - pharmacology
/ endothelial cells
/ Endothelial Cells - drug effects
/ Endothelial Cells - metabolism
/ enzyme inhibitors
/ epoxide hydrolase
/ Epoxide Hydrolases - genetics
/ Epoxide Hydrolases - metabolism
/ Fatty acids
/ Fish oils
/ Fish Oils - chemistry
/ Food Analysis
/ Gene Expression Regulation, Enzymologic - drug effects
/ Genes, Tumor Suppressor
/ Kinases
/ laboratory animals
/ lipid peroxidation
/ metabolites
/ nitric oxide
/ Nuclear Proteins
/ omega-3 fatty acids
/ Oxidative stress
/ p38 Mitogen-Activated Protein Kinases - genetics
/ p38 Mitogen-Activated Protein Kinases - metabolism
/ Polyunsaturated fatty acids
/ Protein expression
/ protein synthesis
/ Proteins
/ Rats
/ Real-Time Polymerase Chain Reaction
/ Renal Artery - cytology
/ RNA, Messenger - genetics
/ RNA, Messenger - metabolism
/ vasodilation
/ Vasodilation - drug effects
/ vasodilator agents
2017
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N-3 Polyunsaturated Fatty Acids Decrease the Protein Expression of Soluble Epoxide Hydrolase via Oxidative Stress-Induced P38 Kinase in Rat Endothelial Cells
by
Okada, Takashi
, Maegawa, Hiroshi
, Imamura, Takeshi
, Morino, Katsutaro
, Kondo, Keiko
, Tawa, Masashi
, Nakagawa, Fumiyuki
, Sekine, Osamu
, Okamura, Tomio
, Ugi, Satoshi
in
Acetylcholine - pharmacology
/ acetylcysteine
/ Animal Feed - analysis
/ Animals
/ Antigens, CD
/ antioxidants
/ aorta
/ Aorta - drug effects
/ arachidonic acid
/ Cadherins
/ cardioprotective effect
/ diet
/ Dietary Supplements
/ docosahexaenoic acid
/ Docosahexaenoic Acids - chemistry
/ Docosahexaenoic Acids - pharmacology
/ eicosapentaenoic acid
/ Eicosapentaenoic Acid - chemistry
/ Eicosapentaenoic Acid - pharmacology
/ endothelial cells
/ Endothelial Cells - drug effects
/ Endothelial Cells - metabolism
/ enzyme inhibitors
/ epoxide hydrolase
/ Epoxide Hydrolases - genetics
/ Epoxide Hydrolases - metabolism
/ Fatty acids
/ Fish oils
/ Fish Oils - chemistry
/ Food Analysis
/ Gene Expression Regulation, Enzymologic - drug effects
/ Genes, Tumor Suppressor
/ Kinases
/ laboratory animals
/ lipid peroxidation
/ metabolites
/ nitric oxide
/ Nuclear Proteins
/ omega-3 fatty acids
/ Oxidative stress
/ p38 Mitogen-Activated Protein Kinases - genetics
/ p38 Mitogen-Activated Protein Kinases - metabolism
/ Polyunsaturated fatty acids
/ Protein expression
/ protein synthesis
/ Proteins
/ Rats
/ Real-Time Polymerase Chain Reaction
/ Renal Artery - cytology
/ RNA, Messenger - genetics
/ RNA, Messenger - metabolism
/ vasodilation
/ Vasodilation - drug effects
/ vasodilator agents
2017
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N-3 Polyunsaturated Fatty Acids Decrease the Protein Expression of Soluble Epoxide Hydrolase via Oxidative Stress-Induced P38 Kinase in Rat Endothelial Cells
by
Okada, Takashi
, Maegawa, Hiroshi
, Imamura, Takeshi
, Morino, Katsutaro
, Kondo, Keiko
, Tawa, Masashi
, Nakagawa, Fumiyuki
, Sekine, Osamu
, Okamura, Tomio
, Ugi, Satoshi
in
Acetylcholine - pharmacology
/ acetylcysteine
/ Animal Feed - analysis
/ Animals
/ Antigens, CD
/ antioxidants
/ aorta
/ Aorta - drug effects
/ arachidonic acid
/ Cadherins
/ cardioprotective effect
/ diet
/ Dietary Supplements
/ docosahexaenoic acid
/ Docosahexaenoic Acids - chemistry
/ Docosahexaenoic Acids - pharmacology
/ eicosapentaenoic acid
/ Eicosapentaenoic Acid - chemistry
/ Eicosapentaenoic Acid - pharmacology
/ endothelial cells
/ Endothelial Cells - drug effects
/ Endothelial Cells - metabolism
/ enzyme inhibitors
/ epoxide hydrolase
/ Epoxide Hydrolases - genetics
/ Epoxide Hydrolases - metabolism
/ Fatty acids
/ Fish oils
/ Fish Oils - chemistry
/ Food Analysis
/ Gene Expression Regulation, Enzymologic - drug effects
/ Genes, Tumor Suppressor
/ Kinases
/ laboratory animals
/ lipid peroxidation
/ metabolites
/ nitric oxide
/ Nuclear Proteins
/ omega-3 fatty acids
/ Oxidative stress
/ p38 Mitogen-Activated Protein Kinases - genetics
/ p38 Mitogen-Activated Protein Kinases - metabolism
/ Polyunsaturated fatty acids
/ Protein expression
/ protein synthesis
/ Proteins
/ Rats
/ Real-Time Polymerase Chain Reaction
/ Renal Artery - cytology
/ RNA, Messenger - genetics
/ RNA, Messenger - metabolism
/ vasodilation
/ Vasodilation - drug effects
/ vasodilator agents
2017
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N-3 Polyunsaturated Fatty Acids Decrease the Protein Expression of Soluble Epoxide Hydrolase via Oxidative Stress-Induced P38 Kinase in Rat Endothelial Cells
Journal Article
N-3 Polyunsaturated Fatty Acids Decrease the Protein Expression of Soluble Epoxide Hydrolase via Oxidative Stress-Induced P38 Kinase in Rat Endothelial Cells
2017
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Overview
N-3 polyunsaturated fatty acids (PUFAs) improve endothelial function. The arachidonic acid-derived metabolites (epoxyeicosatrienoic acids (EETs)) are part of the endothelial hyperpolarization factor and are vasodilators independent of nitric oxide. However, little is known regarding the regulation of EET concentration by docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) in blood vessels. Sprague-Dawley rats were fed either a control or fish oil diet for 3 weeks. Compared with the control, the fish oil diet improved acetylcholine-induced vasodilation and reduced the protein expression of soluble epoxide hydrolase (sEH), a key EET metabolic enzyme, in aortic strips. Both DHA and EPA suppressed sEH protein expression in rat aorta endothelial cells (RAECs). Furthermore, the concentration of 4-hydroxy hexenal (4-HHE), a lipid peroxidation product of n-3 PUFAs, increased in n-3 PUFA-treated RAECs. In addition, 4-HHE treatment suppressed sEH expression in RAECs, suggesting that 4-HHE (derived from n-3 PUFAs) is involved in this phenomenon. The suppression of sEH was attenuated by the p38 kinase inhibitor (SB203580) and by treatment with the antioxidant N-acetyl-L-cysteine. In conclusion, sEH expression decreased after n-3 PUFAs treatment, potentially through oxidative stress and p38 kinase. Mild oxidative stress induced by n-3 PUFAs may contribute to their cardio-protective effect.
Publisher
MDPI AG,MDPI
Subject
/ Animals
/ aorta
/ diet
/ Docosahexaenoic Acids - chemistry
/ Docosahexaenoic Acids - pharmacology
/ Eicosapentaenoic Acid - chemistry
/ Eicosapentaenoic Acid - pharmacology
/ Endothelial Cells - drug effects
/ Endothelial Cells - metabolism
/ Epoxide Hydrolases - genetics
/ Epoxide Hydrolases - metabolism
/ Gene Expression Regulation, Enzymologic - drug effects
/ Kinases
/ p38 Mitogen-Activated Protein Kinases - genetics
/ p38 Mitogen-Activated Protein Kinases - metabolism
/ Proteins
/ Rats
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