Document Detail

Peripheral nerve dysfunction in experimental diabetes is mediated by cyclooxygenase-2 and oxidative stress.
MedLine Citation:
PMID:  16356116     Owner:  NLM     Status:  MEDLINE    
Glucose-mediated oxidative stress and alterations in cyclooxygenase (COX) pathway activity with secondary deficits of endoneurial perfusion have been implicated in the pathogenesis of experimental diabetic neuropathy (EDN). We have previously reported that activation of the COX-2 pathway is an important mediator of neurochemical and neurovascular defects in EDN in a rat model. Considering that chemical COX inhibition may exert other pharmacological effects in addition to inhibition of COX activity, the aim of this study was to explore the role of COX-2 in experimental diabetic neuropathy, using a COX-2 knockout mouse model. Here we provide evidence that COX-2 inactivation had a protective effect against diabetes-induced motor and sensory nerve conduction slowing and impaired nerve antioxidative defense that were clearly manifest in the wild-type (COX-2(+/+)) diabetic mice. These preliminary data support the role of the activation of the COX-2 pathway in mediating sensory and motor nerve conduction velocity deficits in EDN. These findings also suggest that the COX-2 pathway seems to be an important modulator of oxidative stress in EDN.
Aaron P Kellogg; Rodica Pop-Busui
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Antioxidants & redox signaling     Volume:  7     ISSN:  1523-0864     ISO Abbreviation:  Antioxid. Redox Signal.     Publication Date:    2005 Nov-Dec
Date Detail:
Created Date:  2005-12-16     Completed Date:  2006-03-16     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100888899     Medline TA:  Antioxid Redox Signal     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1521-9     Citation Subset:  IM    
Copyright Information:
Antioxid. Redox Signal. 7, 1521-1529.
Medical College of Ohio, Department of Medicine and Physiology, Toledo, OH, USA.
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MeSH Terms
Alkenes / chemistry,  metabolism
Antioxidants / metabolism
Blood Glucose
Body Weight / drug effects,  genetics
Cyclooxygenase 2 / deficiency,  genetics,  metabolism*
Diabetes Mellitus, Experimental / chemically induced,  complications,  enzymology,  physiopathology*
Diabetic Neuropathies / enzymology*,  pathology,  physiopathology*
Enzyme Activation / genetics
Glutathione / metabolism
Lipid Peroxidation / drug effects,  genetics
Malondialdehyde / metabolism
Mice, Knockout
Oxidative Stress*
Peripheral Nerves / enzymology*,  pathology,  physiopathology*
Prostaglandins / metabolism
Streptozocin / pharmacology
Grant Support
Reg. No./Substance:
0/Alkenes; 0/Antioxidants; 0/Blood Glucose; 0/Prostaglandins; 18883-66-4/Streptozocin; 542-78-9/Malondialdehyde; 70-18-8/Glutathione; EC 2

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