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AIM: To investigate protective effects of doxepin (Dox) on cultured neuronal injury induced by oxidative stress. METHODS: Cytotoxicities of glutamate (Glu 0.5 mmol/L, 15 min), sodium dithionite (0.5 mmol/L, 24 h) or hemo- globin (Hb100 mg/L,24 h)and the protective effects of Dox were observed. RESULTS: Exposure of cultured neurons to Glu, sodium dithionite and Hb developed a neurotoxicity expressed in the thiazol blue tetrazolium bro- mide (MTT) assay, the increase of lactate dehydrogenase (LDH) leakage, malondialdehyde (MDA) content and intracellular [Ca2+]i accumulation, as well as the decrease of superoxide dismutase (SOD) activity. DOX 1-100 nmol/L significantly inhibited all above changes. CONCLUSION: Dox protects cultured neurons against oxidative stress-induced injury by suppressing intracellular [Ca2+]iaccumulation, decreasing lipid peroxide generation and stimulating antioxidant enzyme.
METHODS: Cytotoxicities of glutamate (Glu 0.5 mmol / L, 15 min), sodium dithionite (0.5 mmol / L, 24 h) or hemo- RESULTS: Exposure of cultured neurons to Glu, sodium dithionite and Hb developed a neurotoxicity expressed in the thiazol blue tetrazolium bromide (MTT) assay, the globin (Hb 100 mg / L, 24 h) and the protective effects of Dox were observed. increase of lactate dehydrogenase (LDH) leakage and malondialdehyde (MDA) content and intracellular [Ca2 +] i accumulation, as well as the decrease of superoxide dismutase (SOD) activity. DOX 1-100 nmol / L significantly inhibited all above changes. CONCLUSION: Dox protects cultured neurons against oxidative stress-induced injury by damping intracellular [Ca2 +] iaccumulation, decreased lipid peroxide generation and stimulating antioxidant enzyme.