Document Type : Regular Paper
Authors
1
1Department of Pharmacology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
2
Transplant Research Center, Department of pathology, Shiraz University of Medical Sciences, Shiraz, Iran
3
Non-communicable Diseases Research center, Fasa University of Medical Sciences, Fasa, Iran
4
4Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
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5Department of tissue engineering, School of novel sciences and technologies, Shiraz University of Medical Sciences, Shiraz, Iran.
Abstract
Multiple Sclerosis (MS) is a common neuroinflammatory disease causing a wide spectrum of clinical signs and symptoms. Neuropathological changes in MS including inflammation, demyelination and axonal degeneration are seen in the animal counterpart of MS, experimental autoimmune encephalomyelitis (EAE) and are biomarkers to follow the pathophysiology and any pharmacology of MS in experimental studies. To elucidate the pattern of these pathological abnormalities in EAE, different aspects of pathological findings and their correlations were studied in the model. EAE induction was done using MOG in C57/Bl6 mice and H & E, Luxol Fast Blue and Bielschowskey staining were used for histopathological evaluation in each region of the spinal cord, lumbar, thoracic and cervical. There was significant positive correlations between “neurological disease score” in EAE mice and each of these pathological findings: “inflammation score”, “ demyelination score” and “ axonal degeneration”. These correlations were observed regardless of the anatomic regions studied. Inflammation and demyelination scores were significantly associated. Degeneration and demyelination scores were correlated positively also. However, no statistically significant correlation was found between scores of inflammation and degeneration in nether of the three anatomical regions of the spinal cords of EAE mice. This study optimizes the EAE model regarding pathological findings in correlation with neurological deficits in the model. The results will help in better utility of the model in MS research.
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