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• W3029649507 abstract "ObjectiveTo evaluate the potential involvement of melatonin in the activation of nuclear factor-E2-related factor 2-antioxidant response element (Nrf2-ARE) signaling pathway and anti-oxidative stress in an experimental model of traumatic brain injury (TBI).MethodsOne hundred and sixteen ICR male mice, aged 6-8 weeks, were randomly divided into sham-operated group, model group, vehicle group and melatonin treatment group (n=29); mice in the later three groups were established TBI models by Flierl improved free-fall method; 0, 1, 2, 3 and 4 h after that, mice in the melatonin treatment group were performed intraperitoneal injection of melatonin (10 mg/kg, 3 mg/mL diluted in normal saline), and those in the vehicle group were given the same volume of normal saline. Twenty-four h after TBI, the neuronal degeneration was investigated by Fluoro-Jade C (FJC) staining and brain water content was measured by wet-to-dry weight ratio method; colorimetric method was employed to detect the malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels; Western blotting was engaged to analyze the protein content of nuclear Nrf2, cytoplasmic Nrf2, NADPH quinine oxidoreductase-1 (NQO1) and heme oxidase-1 (HO-1); real-time quantitative-PCR was employed to evaluate the mRNA content of HO-1 and NQO-1; electrophoresis mobility shift assay (EMSA) was performed to measure the Nrf2 DNA binding activity.ResultsAs compared with the sham-operated group, the other three groups had significantly increased number of cortical degenerative neurons, water content, MDA content, nuclear Nrf2 expression, and nuclear HO-1 and NQO-1 protein and mRNA expressions, and had significantly lower levels of cytoplasmic Nrf2 and GPx. As compared with the model group and vehicle group, the melatonin treatment group had significantly decreased number of cortical degenerative neurons, water content, MDA content and nuclear Nrf2 expression, and had significantly increased cytoplasmic Nrf2 level, GPx content and nuclear HO-1 and NQO-1 protein and mRNA expressions (P<0.05). The SOD content in the sham-operated group and melatonin treatment group was significantly higher than that in the model group and vehicle group (P<0.05). EMSA showed that the Nrf2 DNA binding activity increased accordingly in the order of sham-operated group, model group, vehicle group and melatonin treatment group.ConclusionThe melatonin can improve the anti-oxidative stress neuroprotection following TBI, which may be associated with the activation of Nrf2-ARE signaling pathway.Key words: Traumatic brain injury; Melatonin; Oxidative stress; Nuclear factor-E2-related factor 2-antioxidant response element" @default.
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• W3029649507 date "2015-04-15" @default.
• W3029649507 modified "2023-09-23" @default.
• W3029649507 title "Role of melatonin in anti-oxidative stress and its mechanism in mice with experimental traumatic brain injury" @default.
• W3029649507 doi "https://doi.org/10.3760/cma.j.issn.1671-8925.2015.04.001" @default.
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