Lithium induced amelioration of a rat model of multiple sclerosis through the suppression of glycogen synthase kinase (GSK)-3 signaling

      Background: Glycogen synthase kinase (GSK)-3 is one of important molecules in the course of cell activation in the central nervous system diseases.
      Objective: The aim of this study was to evaluate whether lithium, an inhibitor of GSK-3 beta, ameliorates rat paralysis with acute monophasic experimental autoimmune encephalomyelitis (EAE).
      Material and Methods: EAE was induced in Lewis rats through immunization of guinea pig myelin basic protein (MBP) and complete Freund’s adjuvant. Lithium was administered in immunized rats.Tissues and sera of rats were collected for the cytokine assay and signals by western blot analysis and immunohistochemistry.
      Results: Lithium treatment significantly delayed the onset of EAE paralysis and ameliorated its severity compared with those of vehicle treated group.
      Conclusion: Taken all into considerations, lithium, an inhibitor of GSK-3 beta, is a potential anti-inflammatory drug to suppress acute autoimmune diseases including rat EAE, possibly through the inactivation of GSK-3 signal cascades. (*supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (Grant number: 2014R1A1A2055965)).