OBJECTIVES: This study tested whether sodium para-amino salicylic dihydrate, an antibacterial drug for tuberculosis, could block manganese-induced apoptosis in SK-N-MC neurons. METHODS: Cell viability, Hoechst staining, dichlorofluorescin diacetate analysis for reactive oxygen species measurement, and immunoblotting were performed. KEY FINDINGS: In vitro, manganese chloride significantly decreased the viability of SK-N-MC cells, accompanied by apoptotic features such as changes in nuclear morphology. Sodium para-amino salicylic dihydrate inhibited these apoptotic characteristics through reducing intracellular reactive oxygen species generation, protecting mitochondrial membrane potential and caspase-3 activation. CONCLUSIONS: Sodium para-amino salicylic dihydrate inhibits manganese-induced apoptosis in neurons and may reduce manganese-mediated neurodegeneration.
OBJECTIVES: This study tested whether sodium para-amino salicylic dihydrate, an antibacterial drug for tuberculosis, could block manganese-induced apoptosis in SK-N-MC neurons. METHODS: Cell viability, Hoechst staining, dichlorofluorescin diacetate analysis for reactive oxygen species measurement, and immunoblotting were performed. KEY FINDINGS: In vitro, manganese chloride significantly decreased the viability of SK-N-MC cells, accompanied by apoptotic features such as changes in nuclear morphology. Sodium para-amino salicylic dihydrate inhibited these apoptotic characteristics through reducing intracellular reactive oxygen species generation, protecting mitochondrial membrane potential and caspase-3 activation. CONCLUSIONS:Sodium para-amino salicylic dihydrate inhibits manganese-induced apoptosis in neurons and may reduce manganese-mediated neurodegeneration.