[SP5-3C-5] Low dose of Diphenyleneiodonium (DPI), specific NADPH oxidase 2 (NOX2) inhibitor, targets NOX2 and ameliorates experimental autoimmune encephalomyelitis (EAE) severity in mouse model
Nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase, NOX), a key superoxide-producing enzyme, plays a critical role in microglia mediated chronic neuroinflammation and subsequent progressive dopaminergic neurodegeneration in Parkinson’s disease. However, seldom articles discuss about the values and effects on different diseases, like experimental autoimmune encephalomyelitis (EAE) in mouse model. The aim of this study was to evaluate the characteristics and effects of low dose of NOX2 inhibitor, diphenyleneiodonium (DPI) in moderate severity of EAE mouse model. Furthermore, we want to ask whether NOX2 knockout mice show disease protection through reducing superoxide and subsequent inflammatory process.
Our preliminary data revealed that pre-treatment with diphenyleneiodonium significantly attenuated progressive encephalomyelitis and reduced the severity of limbs paralysis of mice. Meanwhile, NOX2 knockout mice showed EAE protection through the inhibition of microglial activation and a reduction in the expression of proinflammatory factors.
Our preliminary data revealed that pre-treatment with diphenyleneiodonium significantly attenuated progressive encephalomyelitis and reduced the severity of limbs paralysis of mice. Meanwhile, NOX2 knockout mice showed EAE protection through the inhibition of microglial activation and a reduction in the expression of proinflammatory factors.