Doxepin protects cultured neurons against oxidative stress-induced injury
Abstract
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 hemoglobin (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 bromide (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+]i accumulation, decreasing lipid peroxide generation and stimulating antioxidant enzyme.
Keywords:
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 hemoglobin (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 bromide (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+]i accumulation, decreasing lipid peroxide generation and stimulating antioxidant enzyme.