ABSTRACT
Lutein is known to be a nonprovitamin A carotenoid found in broccoli and spinach. The aim of present study was to investigate whether lutein can protect brain against ischemic injury by reducing oxidative stress. Male ICR mice were randomly divided into five experimental groups: model group, sham group, lutein high, middle, and low-dose groups (30, 15, and 7.5 mg/kg). Mice were subjected to a 2-h middle cerebral artery occlusion followed by reperfusion for 22 h. The reduced glutathione/oxidized glutathione (GSH/GSSG) ratio, antioxidant enzyme activities, malondialdehyde (MDA), and the carbonyl content in oxidatively modified proteins in brain tissue were determined with colorimetric method. The 8-hydroxy deoxyguanosine (8-OHdG) expression was measured by immunohistochemistry assay, and the neuron apoptosis was detected by TdT-mediated dUTP nick end labeling assay. Then, the neurological deficit scores were measured at last. Treatment of lutein significantly elevated the ratio of GSH/GSSG as well as activities of superoxide dismutase, glutathione peroxidase, and catalase and obviously decreased the contents of MDA, brain carbonyl, the expression of 8-OHdG, the number of apoptotic cells, and neurological deficit scores. Our results demonstrate that administration of lutein affords strong neuroprotective effect against transient cerebral ischemic injury and that the effect might be associated with its antioxidant property.
Subject(s)
Ischemic Attack, Transient/drug therapy , Lutein/pharmacology , Neuroprotective Agents/pharmacology , Animals , Antioxidants/pharmacology , Apoptosis/drug effects , Catalase/metabolism , Glutathione Peroxidase/metabolism , Male , Malondialdehyde/pharmacology , Mice , Mice, Inbred ICR , Molecular Structure , Oxidation-Reduction , Oxidative Stress/drug effects , Superoxide Dismutase/metabolismABSTRACT
OBJECTIVE: To investigate the effect of Astaxanthin on enhancing the function of anti-oxidative damage in osteoblast. METHODS: MC3T3-E1 osteoblasts were randomly divided into five groups, including control group, model group, Astaxanthin group [low-dose (1 x 10(-7) mol/L), middle-dose (1 x 10(-6) mol/L), high-dose (1 x 10(-5) mol/L)], in which the activity of cells, activity of superoxide dismutase (SOD), the content of reactive oxygen species (ROS), lipid oxygen (LPO) and membrane fluidity were tested and compared. RESULTS: Compared with Astaxanthin groups, the activity of cells, SOD activity and membrane fluidity in the model group were significantly decreased (P < 0.01). However, the contents of ROS and LPO were significantly raised (P < 0.01). CONCLUSION: H2O2 can cause oxidative damage of MC3T3-E1 osteoblasts, but Astaxanthin can prevent or decrease its influence.
Subject(s)
Antioxidants/pharmacology , Hydrogen Peroxide/metabolism , Osteoblasts/drug effects , Oxidative Stress/drug effects , Animals , Antioxidants/chemistry , Cell Line , Lipid Peroxidation/drug effects , Membrane Fluidity/drug effects , Mice , Osteoblasts/metabolism , Reactive Oxygen Species/metabolism , Superoxide Dismutase/metabolism , Xanthophylls/chemistry , Xanthophylls/pharmacologyABSTRACT
OBJECTIVE: To study the influence of canthaxanthin on D-galactose induced osseous changes of rat. METHODS: Forty-five six-week-old Wistar male rats were randomly divided into model group, canthaxanthin group and young control group. In addition, 15 sixteen-month-old Wistar male rats were used as old control group. Model group and canthaxanthin group were given injections of D-galactose for 5 months (20 mg/kg/once per-day) to cause aging of rat. Then routine osseous parameters were tested and compared among the 4 groups. RESULTS: Compared with young control group, the BMD, parameters of structural mechanics and biomechanics, bone calcium, manganese, magnesium and the content of hydroxyproline in the model group decreased significantly (P < 0.01), however, the content of bone phosphorus, the activity of bone and serum ALP increased significantly (P < 0.01). Those changes of the model group were the same as the old control group,but the changes in the canthaxanthin group significantly differed with the model group (P < 0.01). CONCLUSION: The high does of D-galactose intake can cause aging and osteoporosis at the same time in rat, but canthaxanthin can prevent and inhibit D-galactose induced osseous changes.
