ABSTRACT
<p><b>OBJECTIVE</b>To study the protective effects of N-acetylcysteine (NAC) against oxidative injury in the brain tissue of mice induced by decabromodiphenyl ether (PBDE-209) and the expression of mitogen activated protein kinase (MAPK)-related proteins in the hippocampus.</p><p><b>METHODS</b>Twenty-one male BALB/c mice were randomly divided into three groups with seven mice in each group: solvent control group, PBDE-209 group with gavage of 500 mg/kg PBDE-209, and PBDE-209 +NAC group which received intraperitoneal injection of 100 mg/kg NAC 0.5 h before exposure to PBDE-209. Mice were sacrificed 6 weeks after exposure. Malondialdehyde (MDA) level, superoxide dismutase (SOD) activity, and glutathione (GSH) level in the cerebral cortex, hippocampus, cerebellum, and striatum, as well as the protein expression of extracellular signal-regulated kinase (ERK), phosphorylated ERK (p-ERK), p38 MAPK (p38), and phosphorylated p38 (p-p38) in the hippocampus, were determined by Western blot.</p><p><b>RESULTS</b>Compared with the hippocampal and cerebellar levels of MDA in control group [(4.91±1.60) and (2.42±1.41) nmol/mg pro] and PBDE-209+NAC group [(6.16±1.03) and (2.83±0.85) nmol/mg pro], the MDA levels in PBDE-209 group [(12.12±6.39) and (4.24±1.15) nmol/mg pro] were significantly increased (P < 0.05). The striatum MDA level in PBDE-209 group [(12.92±4.30) nmol/mg pro] was significantly increased as compared with that of the control group [(4.05±2.23) nmol/mg pro] (P < 0.05). The hippocampal SOD activity of PBDE-209 group [(59.29±37.09) U/mg pro] was reduced significantly as compared with those of the control group [(93.28±21.75) U/mg pro] and PBDE-209+NAC group [(98.92±21.54) U/mgpro] (P < 0.05). The GSH levels in the cerebral cortex, striatum, and cerebellum in PBDE-209 group [(40.98±13.19), (24.46±11.30), and (3.55±1.55) mg GSH/g pro] were significantly reduced as compared with those of the control group [(75.79±26.51), (44.52±13.15) and (8.01±3.23) mg GSH/g pro] and the PBDE-209+NAC group [(89.86±28.39), (39.01±9.05) and (10.34±2.58) mg GSH/g pro] (P < 0.05). Western blot results showed that the ratios of p-p38/p38 and p-ERK/ERK in the hippocampus were significantly higher in the PBDE-209 group than in the control group and PBDE-209+NAC group (P < 0.05).</p><p><b>CONCLUSION</b>Antioxidant NAC has a protective effect against PBDE-209-induced brain injury in mice to some extent, and reduces the expression of MAPK-related proteins.</p>
Subject(s)
Animals , Male , Acetylcysteine , Pharmacology , Antioxidants , Metabolism , Pharmacology , Brain , Metabolism , Extracellular Signal-Regulated MAP Kinases , Metabolism , Glutathione , Metabolism , Halogenated Diphenyl Ethers , Toxicity , Hippocampus , Metabolism , Malondialdehyde , Metabolism , Mice, Inbred BALB C , Mitogen-Activated Protein Kinases , Metabolism , Oxidation-Reduction , Phosphorylation , p38 Mitogen-Activated Protein Kinases , MetabolismABSTRACT
Objective To investigate the serum level of C-reactive protein (CRP) in patients with cerebral infarction and its effect on the prognosis of brain infarction.Methods 113 patients (86 with thrombosis and 27 with lacunar infarction) and 48 healthy persons as control were enrolled in this study. The serum level and abnormal rate of CRP were determined. All the patients were scored by clinic neurological function deficit scale (NDS).Results The serum level of CRP in the patients with thrombosis was higher than that in the patients with lacunar infarction. It was also higher in the patients with lacunar infarction than in normal controls (all P
ABSTRACT
Reports said formaldehyde could induce the damages of organism and cause the peroxidation of lipids. Formaldehyde inhalation may significantly increase the tissue malondialdehyde concentration and decrease the activity of superoxide dismutase, catalase enzyme, glutathione peroxidase enzyme and the concentration of glutathione in the tissues with a dose-effect relationship. The possible mechanisms of oxidation lesion and the toxic effects of formaldehyde were discussed in the present paper.
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Objective To investigate the indoors air formaldehyde pollution in the human anatomy laboratory and its effects on students health. Methods AHMT method was used to determine the concentration of formaldehyde in the indoor air and to observe the students’ signs and symptoms in the near month. Results The level of formaldehyde in the air of human anatomy laboratory was higher than that of the control and was higher than national standard limit. The prevalence rate of eye symptoms(51.98%), nasal symptoms(58.91%), throat symptoms(48.02%), nausea and vomiting, psychiatric symptoms(68.32%) and cold liability (60.89%) in the exposed group was higher than those in the control group(P