Zeaxanthin improves diabetes-induced cognitive deficit in rats through activiting PI3K/AKT signaling pathway

•Diabetes- induced cognitive deficit could be ameliorated by zeaxanthin.•Zeaxanthin could protect hippocampal neurons against hyperglycemia.•Zeaxanthin improved cognitive deficit through activating PI3K/AKT signaling pathway. Published studies have shown that cognitive deficit is a characteristic ma...

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Published inBrain research bulletin Vol. 132; pp. 190 - 198
Main Authors Zhou, Xiaoyan, Wang, Shanshan, Ding, Xin, Qin, Li, Mao, Yizhen, Chen, Lei, Li, Wei, Ying, Changjiang
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.06.2017
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Abstract •Diabetes- induced cognitive deficit could be ameliorated by zeaxanthin.•Zeaxanthin could protect hippocampal neurons against hyperglycemia.•Zeaxanthin improved cognitive deficit through activating PI3K/AKT signaling pathway. Published studies have shown that cognitive deficit is a characteristic manifestation of neurodegenerative disease in diabetes. However, there is no effective prevention and treatment for this diabetes-associated behavior disorder. In the present study, we attempted to elucidate the effect of zeaxanthin on cognitive deficit and the change in the hippocampus correlated with cognitive decline in diabetic rats. Diabetic rats in this study were induced by high-fat diet and low-dose streptozocin (STZ), cognitive ability of rats were evaluated use morris water maze (MWM) and morphology change in hippocampus was assessed by cresyl violet stain. Moreover, we detected the expression of phosphorylated serine/threonine kinase (p-AKT) and Cleaved caspase-3, and the activity of nuclear factor-κB (NF-κB) use western-blot (WB). Results displayed that supplementation with zeaxanthin reduce blood glucose, improve cognitive deficit, survive neural cell, increase p-AKT level, inhibit Cleaved caspase-3 level and NF-κB nuclear transcription in hippocampus. This study demonstrated that zeaxanthin ameliorate diabetes-related cognitive deficit may by means of protecting neural cell from hyperglycemia involved in AKT/NF-κB signaling pathway. This study may provide a potential therapeutic approach for the prevention of diabetes- associated cognitive deficit.
AbstractList •Diabetes- induced cognitive deficit could be ameliorated by zeaxanthin.•Zeaxanthin could protect hippocampal neurons against hyperglycemia.•Zeaxanthin improved cognitive deficit through activating PI3K/AKT signaling pathway. Published studies have shown that cognitive deficit is a characteristic manifestation of neurodegenerative disease in diabetes. However, there is no effective prevention and treatment for this diabetes-associated behavior disorder. In the present study, we attempted to elucidate the effect of zeaxanthin on cognitive deficit and the change in the hippocampus correlated with cognitive decline in diabetic rats. Diabetic rats in this study were induced by high-fat diet and low-dose streptozocin (STZ), cognitive ability of rats were evaluated use morris water maze (MWM) and morphology change in hippocampus was assessed by cresyl violet stain. Moreover, we detected the expression of phosphorylated serine/threonine kinase (p-AKT) and Cleaved caspase-3, and the activity of nuclear factor-κB (NF-κB) use western-blot (WB). Results displayed that supplementation with zeaxanthin reduce blood glucose, improve cognitive deficit, survive neural cell, increase p-AKT level, inhibit Cleaved caspase-3 level and NF-κB nuclear transcription in hippocampus. This study demonstrated that zeaxanthin ameliorate diabetes-related cognitive deficit may by means of protecting neural cell from hyperglycemia involved in AKT/NF-κB signaling pathway. This study may provide a potential therapeutic approach for the prevention of diabetes- associated cognitive deficit.
Highlights • Diabetes- induced cognitive deficit could be ameliorated by zeaxanthin. • Zeaxanthin could protect hippocampal neurons against hyperglycemia. • Zeaxanthin improved cognitive deficit through activating PI3K/AKT signaling pathway.
Published studies have shown that cognitive deficit is a characteristic manifestation of neurodegenerative disease in diabetes. However, there is no effective prevention and treatment for this diabetes-associated behavior disorder. In the present study, we attempted to elucidate the effect of zeaxanthin on cognitive deficit and the change in the hippocampus correlated with cognitive decline in diabetic rats. Diabetic rats in this study were induced by high-fat diet and low-dose streptozocin (STZ), cognitive ability of rats were evaluated use morris water maze (MWM) and morphology change in hippocampus was assessed by cresyl violet stain. Moreover, we detected the expression of phosphorylated serine/threonine kinase (p-AKT) and Cleaved caspase-3, and the activity of nuclear factor-κB (NF-κB) use western-blot (WB). Results displayed that supplementation with zeaxanthin reduce blood glucose, improve cognitive deficit, survive neural cell, increase p-AKT level, inhibit Cleaved caspase-3 level and NF-κB nuclear transcription in hippocampus. This study demonstrated that zeaxanthin ameliorate diabetes-related cognitive deficit may by means of protecting neural cell from hyperglycemia involved in AKT/NF-κB signaling pathway. This study may provide a potential therapeutic approach for the prevention of diabetes- associated cognitive deficit.Published studies have shown that cognitive deficit is a characteristic manifestation of neurodegenerative disease in diabetes. However, there is no effective prevention and treatment for this diabetes-associated behavior disorder. In the present study, we attempted to elucidate the effect of zeaxanthin on cognitive deficit and the change in the hippocampus correlated with cognitive decline in diabetic rats. Diabetic rats in this study were induced by high-fat diet and low-dose streptozocin (STZ), cognitive ability of rats were evaluated use morris water maze (MWM) and morphology change in hippocampus was assessed by cresyl violet stain. Moreover, we detected the expression of phosphorylated serine/threonine kinase (p-AKT) and Cleaved caspase-3, and the activity of nuclear factor-κB (NF-κB) use western-blot (WB). Results displayed that supplementation with zeaxanthin reduce blood glucose, improve cognitive deficit, survive neural cell, increase p-AKT level, inhibit Cleaved caspase-3 level and NF-κB nuclear transcription in hippocampus. This study demonstrated that zeaxanthin ameliorate diabetes-related cognitive deficit may by means of protecting neural cell from hyperglycemia involved in AKT/NF-κB signaling pathway. This study may provide a potential therapeutic approach for the prevention of diabetes- associated cognitive deficit.
Published studies have shown that cognitive deficit is a characteristic manifestation of neurodegenerative disease in diabetes. However, there is no effective prevention and treatment for this diabetes-associated behavior disorder. In the present study, we attempted to elucidate the effect of zeaxanthin on cognitive deficit and the change in the hippocampus correlated with cognitive decline in diabetic rats. Diabetic rats in this study were induced by high-fat diet and low-dose streptozocin (STZ), cognitive ability of rats were evaluated use morris water maze (MWM) and morphology change in hippocampus was assessed by cresyl violet stain. Moreover, we detected the expression of phosphorylated serine/threonine kinase (p-AKT) and Cleaved caspase-3, and the activity of nuclear factor-κB (NF-κB) use western-blot (WB). Results displayed that supplementation with zeaxanthin reduce blood glucose, improve cognitive deficit, survive neural cell, increase p-AKT level, inhibit Cleaved caspase-3 level and NF-κB nuclear transcription in hippocampus. This study demonstrated that zeaxanthin ameliorate diabetes-related cognitive deficit may by means of protecting neural cell from hyperglycemia involved in AKT/NF-κB signaling pathway. This study may provide a potential therapeutic approach for the prevention of diabetes- associated cognitive deficit.
Author Mao, Yizhen
Zhou, Xiaoyan
Wang, Shanshan
Ying, Changjiang
Chen, Lei
Li, Wei
Ding, Xin
Qin, Li
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Keywords Zeaxanthin
NF-κB
AKT
Diabetes
Cognitive deficit
Language English
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Snippet •Diabetes- induced cognitive deficit could be ameliorated by zeaxanthin.•Zeaxanthin could protect hippocampal neurons against hyperglycemia.•Zeaxanthin...
Highlights • Diabetes- induced cognitive deficit could be ameliorated by zeaxanthin. • Zeaxanthin could protect hippocampal neurons against hyperglycemia. •...
Published studies have shown that cognitive deficit is a characteristic manifestation of neurodegenerative disease in diabetes. However, there is no effective...
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SubjectTerms Active Transport, Cell Nucleus - drug effects
Active Transport, Cell Nucleus - physiology
AKT
Animals
Caspase 3 - metabolism
Cell Survival - drug effects
Cell Survival - physiology
Cognition Disorders - drug therapy
Cognition Disorders - enzymology
Cognition Disorders - etiology
Cognition Disorders - pathology
Cognitive deficit
Diabetes
Diabetes Mellitus, Experimental - drug therapy
Diabetes Mellitus, Experimental - enzymology
Diabetes Mellitus, Experimental - pathology
Diabetes Mellitus, Experimental - psychology
Hippocampus - drug effects
Hippocampus - enzymology
Hippocampus - pathology
Hypoglycemic Agents - chemistry
Hypoglycemic Agents - pharmacology
Male
Maze Learning - drug effects
Maze Learning - physiology
Neurology
Neurons - drug effects
Neurons - enzymology
Neurons - pathology
Neuroprotective Agents - chemistry
Neuroprotective Agents - pharmacology
NF-kappa B - metabolism
NF-κB
Nootropic Agents - chemistry
Nootropic Agents - pharmacology
Phosphatidylinositol 3-Kinases - metabolism
Proto-Oncogene Proteins c-akt - metabolism
Rats, Sprague-Dawley
Signal Transduction - drug effects
Zeaxanthin
Zeaxanthins - chemistry
Zeaxanthins - pharmacology
Title Zeaxanthin improves diabetes-induced cognitive deficit in rats through activiting PI3K/AKT signaling pathway
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0361923016304695
https://www.clinicalkey.es/playcontent/1-s2.0-S0361923016304695
https://dx.doi.org/10.1016/j.brainresbull.2017.06.001
https://www.ncbi.nlm.nih.gov/pubmed/28599877
https://www.proquest.com/docview/1908430267
Volume 132
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