Depletion of glutathione induced apoptosis and oxidative stress via the activation of TRPM2 channels in the microglia cells with Alzheimer’ disease model

Alzheimer’s disease is a common neurodegenerative disease. Microglia induces oxidative stress in the brain for engulfing bacteria and viruses. The accumulating data indicate that apoptosis are two main actors induction of microglia activation-induced Disease. Oxidative one many triggers activate transient receptor potential melastatin 2 (TRPM2) channel. Glutathione (GSH) cytosolic antioxidant mammalian cells. GSH depletion via activation TRPM2 neuronal It has not yet been researched how affects microglial cells with Alzheimer's model. BV2 divided into 5 groups as control, buthionine sulphoximine (BSO 0.5 mM 6 h), amyloid beta (1 uM 72 beta+BSO, beta+BSO+GSH (10 h). In BSO group, levels apoptosis, mitochondrial membrane potential, free oxygen reactive species (cyROS), caspase (Casps) -3, Casps -8, -9 were increased compared to control although cell viability level was decreased. expression TRPM2, -9, Bax, Bcl-2, PARP-1 also group. addition, their further BSO+amyloid However, changes modulated beta+GSH group by incubation GSH. conclusion, cyROS caspases beta-induced treatment may be target on