Endoplasmic Reticulum Stress-Mediated Hippocampal Neuron Apoptosis Involved in Diabetic Cognitive Impairment

Poor management of DM causes cognitive impairment while the mechanism is still unconfirmed. The aim of the present study was to investigate the activation of C/EBP Homology Protein (CHOP), the prominent mediator of the endoplasmic reticulum (ER) stress-induced apoptosis under hyperglycemia. We emplo...

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Bibliographic Details
Published in:BioMed research international 2013-01, Vol.2013 (2013), p.1-9
Main Authors: Ling, Shucai, He, Daqiang, Xu, Linhao, Zhang, Xiaoming
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - genetics
Caspase 12 - metabolism
Cells, Cultured
Cognitive Dysfunction - complications
Cognitive Dysfunction - metabolism
Cognitive Dysfunction - physiopathology
Diabetes
Diabetes Mellitus, Experimental - complications
Diabetes Mellitus, Experimental - pathology
Endoplasmic Reticulum Stress
Hippocampus - pathology
Hippocampus - ultrastructure
Humans
Hyperglycemia
Hyperglycemia - complications
Hyperglycemia - pathology
Immunohistochemistry
Kinases
Male
Metabolic disorders
Neurons - metabolism
Neurons - pathology
Neurons - ultrastructure
Rats
Rodents
Synapses - metabolism
Synapses - ultrastructure
Transcription Factor CHOP - metabolism
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Summary:Poor management of DM causes cognitive impairment while the mechanism is still unconfirmed. The aim of the present study was to investigate the activation of C/EBP Homology Protein (CHOP), the prominent mediator of the endoplasmic reticulum (ER) stress-induced apoptosis under hyperglycemia. We employed streptozotocin- (STZ-) induced diabetic rats to explore the ability of learning and memory by the Morris water maze test. The ultrastructure of hippocampus in diabetic rats and cultured neurons in high glucose medium were observed by transmission electron microscopy and scanning electron microscopy. TUNEL staining was also performed to assess apoptotic cells while the expression of CHOP was assayed by immunohistochemistry and Western blot assay in these hippocampal neurons. Six weeks after diabetes induction, the escape latency increased and the average frequency in finding the platform decreased in diabetic rats (P
ISSN:2314-6133
2314-6141
DOI:10.1155/2013/924327