METFORMIN PROMOTES AUTOPHAGY IN GLIAL CELLS AND REDUCES NEUROINFLAMMATION IN EXPERIMENTAL MODELS OF TYPE 2 DIABETES MELLITUS

GONZALEZ PEREZ N; POMILIO C; VINUESA A; BELLOTTO M; BENTIVEGNA M; GREGOSA A; PRESA J; BEAUQUIS J; SARAVIA F

Mar del Plata

Congreso; Reunión Anual de Sociedades de Biociencias; 2022

Sociedad Argentina de Investigación Clínica (SAIC)

Drug repositioning is a strategy for identifying new uses for approvedsafe drugs that are outside the scope of the original medicalindication. Pathological chronic activation of the brain immune responseand autophagy impairment frequently occur in associationwith aging and is exacerbated in age-related diseases, like type 2 diabetes(T2D) and Alzheimer’s disease. Here, we tested the potentialtherapeutic role of metformin –the first-line drug used for treatmentin T2D– in reducing neuroinflammation and restoring autophagicflux in astrocytes and microglia. Our preliminary results employingcell lines showed no effect of metformin on viability; astrocytic cellsexposed to 0,2 mM metformin during 2 h showed an increased immunoreactivityfor the autophagy marker LC3; while microglial cellsexposed 30 min to this concentration exhibited increased autophagy,evaluated by western blot against LC3 and the autphagy-specificsubstract p62 (p