Abstract

Multiple sclerosis (MS) is a chronic neuroinflammatory demyelinating disorder of the central nervous system with unclear exact etiology. The experimental autoimmune encephalomyelitis (EAE) model in C57BL/6 mice is the most common animal model for MS sharing many clinical and pathophysiological features to expand our knowledge on the pathophysiology of the disease and to develop novel treatment strategies. The current study was planned to evaluate the effect of EAE on hematologic and plasma total protein and albumin levels in C57BL/6 mice.
 EAE was induced with myelin oligodendrocyte glycoprotein (MOG35-55) peptide in the female C57BL/6 mice. The EAE clinically caused paralyzed tail, hind limb paresis, and uncoordinated movement in the mice. The EAE-induced mice hematologically had a mild increase in white blood cell count without altering neutrophil-lymphocyte ratio but no change in vital hematological parameters such as red blood cell count, packed cell volume, and hemoglobin level. Moreover, the EAE produced a rise in the plasma total protein level and an attenuation in plasma albumin level in the mice.
 In conclusion, our findings show that the EAE model in mice might not cause any significant change hematologically, except a slight increase in the white blood cell count, and might produce changes in the plasma protein level. The EAE-induced blood parameter effects, as the findings of the current study, could take consideration in terms of understanding the pathophysiology of the disease and developing a novel therapeutic approach for the disease.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call