Document Type : Original Article
Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran;Department of Brain and Cognitive Sciences, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology,
Multiple sclerosis (MS) is a demyelinating disease of the central nervous system. The autoimmune pathology and long-term inflammation lead to substantial demyelination. These events lead to a substantial loss of oligodendrocytes (OLs), which in a longer period, results in axonal loss and long-term disabilities. Neural cells protection approaches decelerate or inhibit the disease progress to avoid further disability. Previous studies showed that metformin has beneficial effects against neurodegenerative conditions. In this experimental study, we examined possible protective effects of metformin on toxin-induced myelin destruction in adult mice brains.
Materials and Methods
Lysophosphatidylcholine (LPC) was used to induce demyelination in mice optic chiasm. We examined the extent of demyelination at different time points post LPC injection using myelin staining and evaluated the severity of inflammation. Functional state of optic pathway was evaluated by visual evoked potential (VEP) recording.
Metformin attenuated LPC-induced demyelination (P < 0.05) and inflammation (P < 0.05) and protected against significant decrease (P < 0.05) in functional conductivity of optic tract. These data indicated that metformin administration attenuates the myelin degeneration following LPC injection which led to functional enhancement.
Our findings suggest metformin for combination therapy for patients suffering from the myelin degenerative diseases, especially multiple sclerosis; however, additional mechanistic studies are required.