Inhibitory effects of omega-3 fatty acids on early brain injury after subarachnoid hemorrhage in rats: Possible involvement of G protein-coupled receptor 120/β-arrestin2/TGF-β activated kinase-1 binding protein-1 signaling pathway. (June 2016)
- Record Type:
- Journal Article
- Title:
- Inhibitory effects of omega-3 fatty acids on early brain injury after subarachnoid hemorrhage in rats: Possible involvement of G protein-coupled receptor 120/β-arrestin2/TGF-β activated kinase-1 binding protein-1 signaling pathway. (June 2016)
- Main Title:
- Inhibitory effects of omega-3 fatty acids on early brain injury after subarachnoid hemorrhage in rats: Possible involvement of G protein-coupled receptor 120/β-arrestin2/TGF-β activated kinase-1 binding protein-1 signaling pathway
- Authors:
- Yin, Jia
Li, Haiying
Meng, Chengjie
Chen, Dongdong
Chen, Zhouqing
Wang, Yibin
Wang, Zhong
Chen, Gang - Abstract:
- Highlights: Omega-3 fatty acids inhibit post-SAH EBI via GPR 120/β-arrestin2/TAB1. Fish omega-3 fatty acids as part of a daily diet may reduce post-SAH EBI. GPR120 may serve as a new target for prevention and treatment of post-SAH EBI. Abstract: Omega-3 fatty acids have been reported to improve neuron functions during aging and in patients affected by mild cognitive impairment, and mediate potent anti-inflammatory via G protein-coupled receptor 120 (GPR120) signal pathway. Neuron dysfunction and inflammatory response also contributed to the progression of subarachnoid hemorrhage (SAH)-induced early brain injury (EBI). This study was to examine the effects of omega-3 fatty acids on SAH-induced EBI. Two weeks before SAH, 30% Omega-3 fatty acids was administered by oral gavage at 1 g/kg body weight once every 24 h. Specific siRNA for GPR120 was exploited. Terminal deoxynucleotidyl transferase dUTP nick end labeling, fluoro-Jade B staining, and neurobehavioral scores and brain water content test showed that omega-3 fatty acids effectively suppressed SAH-induced brain cell apoptosis and neuronal degradation, behavioral impairment, and brain edema. Western blot, immunoprecipitation, and electrophoretic mobility shift assays results showed that omega-3 fatty acids effectively suppressed SAH-induced elevation of inflammatory factors, including cyclooxygenase-2, monocyte chemoattractant protein-1, and inducible nitric oxide synthase. In addition, omega-3 fatty acids could inhibitHighlights: Omega-3 fatty acids inhibit post-SAH EBI via GPR 120/β-arrestin2/TAB1. Fish omega-3 fatty acids as part of a daily diet may reduce post-SAH EBI. GPR120 may serve as a new target for prevention and treatment of post-SAH EBI. Abstract: Omega-3 fatty acids have been reported to improve neuron functions during aging and in patients affected by mild cognitive impairment, and mediate potent anti-inflammatory via G protein-coupled receptor 120 (GPR120) signal pathway. Neuron dysfunction and inflammatory response also contributed to the progression of subarachnoid hemorrhage (SAH)-induced early brain injury (EBI). This study was to examine the effects of omega-3 fatty acids on SAH-induced EBI. Two weeks before SAH, 30% Omega-3 fatty acids was administered by oral gavage at 1 g/kg body weight once every 24 h. Specific siRNA for GPR120 was exploited. Terminal deoxynucleotidyl transferase dUTP nick end labeling, fluoro-Jade B staining, and neurobehavioral scores and brain water content test showed that omega-3 fatty acids effectively suppressed SAH-induced brain cell apoptosis and neuronal degradation, behavioral impairment, and brain edema. Western blot, immunoprecipitation, and electrophoretic mobility shift assays results showed that omega-3 fatty acids effectively suppressed SAH-induced elevation of inflammatory factors, including cyclooxygenase-2, monocyte chemoattractant protein-1, and inducible nitric oxide synthase. In addition, omega-3 fatty acids could inhibit phosphorylation of transforming growth factor β activated kinase-1 (TAK1), MEK4, c-Jun N-terminal kinase, and IkappaB kinase as well as activation of nuclear factor kappa B through regulating GPR120/β-arrestin2/TAK1 binding protein-1 pathway. Furthermore, siRNA-induced GPR120 silencing blocked the protective effects of omega-3 fatty acids. Here, we show that stimulation of GPR120 with omega-3 fatty acids pretreatment causes anti-apoptosis and anti-inflammatory effects via β-arrestin2/TAK1 binding protein-1/TAK1 pathway in the brains of SAH rats. Fish omega-3 fatty acids as part of a daily diet may reduce EBI in an experimental rat model of SAH. … (more)
- Is Part Of:
- International journal of biochemistry & cell biology. Volume 75(2016:Jun.)
- Journal:
- International journal of biochemistry & cell biology
- Issue:
- Volume 75(2016:Jun.)
- Issue Display:
- Volume 75 (2016)
- Year:
- 2016
- Volume:
- 75
- Issue Sort Value:
- 2016-0075-0000-0000
- Page Start:
- 11
- Page End:
- 22
- Publication Date:
- 2016-06
- Subjects:
- COX-2 cyclooxygenase-2 -- DAPI 4, 6-diamino-2-phenyl indole -- DHA docosahexaenoic acid -- EBI early brain injury -- EMSA electrophoretic mobility shift assays -- EPA eicosapentaenoic acid -- FJB Fluoro-Jade B -- GAPDH glyceraldehyde-3-phosphate dehydrogenase -- GPR120 G protein-coupled receptor 120 -- IKK IkappaB kinase -- iNOS inducible nitric oxide synthase -- JNK c-Jun N-terminal kinase -- MCP-1 monocyte chemoattractant protein-1 -- NF-κB nuclear factor kappa B -- SAH subarachnoid hemorrhage -- SD Sprague Dawley -- TAK1 transforming growth factor β activated kinase-1 -- TUNEL terminal deoxynucleotidyl transferase dUTP nick end labeling -- ω-3 omega-3 fatty acids
Apoptosis -- Early brain injury -- G protein-coupled receptor 120 -- Omega-3 fatty acids -- Subarachnoid hemorrhage
Biochemistry -- Periodicals
Cytology -- Periodicals
Biochemistry -- Periodicals
Cell Biology -- Periodicals
Biochimie -- Périodiques
Cytologie -- Périodiques
Biochimie
Cytologie
Biochemistry
Cytology
Ressource Internet (Descripteur de forme)
Périodique électronique (Descripteur de forme)
Periodicals
572.05 - Journal URLs:
- http://www.sciencedirect.com/science/journal/13572725 ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.biocel.2016.03.008 ↗
- Languages:
- English
- ISSNs:
- 1357-2725
- Deposit Type:
- Legaldeposit
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- British Library DSC - 4542.135000
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