Methylprednisolone reduces axonal impairment in the experimental model of brain oedema

In our earlier paper we demonstrated that opening of the blood-brain barrier with an osmotic insult induces brain oedema which represents a factor triggering axonal impairment accompanied with myelin disintegration. The aim of the present study was to find whether methylprednisolone can reduce such axonal impairment in our model of brain oedema.

Brain oedema was induced by osmotic blood-brain barrier opening with 20% mannitol applied selectively into the internal carotid. Axonal changes were recognized as signs of myelin disintegration (oedematous vesicles, varicosity, myelin fragmentation) at histological sections stained with Black Gold in hippocampal areas CA1 and CA3 and in the dentate gyrus at time intervals of 30 minutes (acute group) or one week (chronic group) after the blood-brain barrier opening. At the same time intervals methylprednisolone was applied in two different ways - into peritoneal cavity or into the right carotid artery.

Impairment of the axonal integrity (changes of the myelin sheet integrity) was identified in all areas studied in both experimental groups. Whereas in the control group axons were of the uniform diameter, in the experimental groups various forms of myelin disintegration were observed. Methylprednisolone reduced the degree of myelin disintegration in both time intervals with the highest effect in the acute group with the intracarotic administration.

Methylprednisolone can effectively reduce myelin changes accompanying brain oedema induced by blood-brain barrier opening with an osmotic insult.