Brown algae are well known as a source of biologically active compounds, especially those having antioxidant activities, such as phlorotannins. In this study we examined the antioxidant activities of crude phlorotannins extracts (CPEs) obtained from Sargassum hemiphyllum (SH) and fractionated according to the molecular weights. When CPEs were administrated at a dose of 30 mg/kg to Kunming mice pre-treated with carbon tetrachloride (CCl4), the levels of oxidative stress indicators in the liver, kidney and brain were significantly reduced in vivo. All the components of various molecular weight fractions of CPEs exhibited greater scavenging capacities in clearing hydroxyl free radical and superoxide anion than the positive controls gallic acid, vitamin C and vitamin E. Particularly, the components greater than 30 kD obtained from ethyl acetate phase showed the highest antioxidant capacities. These results indicated that SH is a potential source for extracting phlorotannins, the algal antioxidant compounds.
Animals ; Antioxidants ; isolation & purification ; pharmacology ; Ascorbic Acid ; pharmacology ; Brain ; drug effects ; metabolism ; pathology ; Carbon Tetrachloride ; antagonists & inhibitors ; toxicity ; Carbon Tetrachloride Poisoning ; drug therapy ; metabolism ; pathology ; Chemical Fractionation ; methods ; Gallic Acid ; pharmacology ; Hydroxyl Radical ; antagonists & inhibitors ; metabolism ; Kidney ; drug effects ; metabolism ; pathology ; Liquid-Liquid Extraction ; methods ; Liver ; drug effects ; metabolism ; pathology ; Male ; Mice ; Mice, Inbred Strains ; Oxidation-Reduction ; Oxidative Stress ; drug effects ; Phaeophyta ; chemistry ; Sargassum ; chemistry ; Superoxides ; antagonists & inhibitors ; metabolism ; Tannins ; isolation & purification ; pharmacology ; Vitamin E ; pharmacology

DWP208 is a sodium succinate form of ZYM-201 which is a triterpenoid glycoside isolated from Sanguisorba officinalis, a medicinal plant prescribed for various diseases, such as duodenal ulcers and bleeding in East Asian counties. We demonstrated that this compound is able to normalize the altered lipid metabolism induced by hyperglycemia and a high fat diet. In this study, we determined whether hyperlipidemic conditions induced with chronically treated alcohol can also be restored by DWP208. Similar to our previous results, orally administered DWP208 (1 to 10 mg/kg) also ameliorated the hyperlipidemia that was induced by alcohol. This compound reversed the alcohol-induced hyperlipidemia including (i) up-regulated hyperlipidemic parameters such as low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), atherosclerotic index (AI), triglyceride, and total cholesterol, and (ii) down-regulated hyperlipidemic parameters such as absolute body weight, superoxide dismutase (SOD) activity, and high-density lipoprotein (HDL) in serum and liver. According to our data, the ameliorative activity of DWP208 is due to its indirect anti-oxidative activity as a result of which lipid peroxide and hydroxyl radical levels were reduced and the activity of SOD was enhanced. Therefore, our data strongly suggest that DWP208 can be used as a remedy against alcohol-induced hyperlipidemia.
Asian Continental Ancestry Group ; Body Weight ; Cholesterol ; Diet, High-Fat ; Duodenal Ulcer ; Hemorrhage ; Humans ; Hydroxyl Radical ; Hyperglycemia ; Hyperlipidemias* ; Lipid Metabolism ; Lipoproteins ; Liver ; Plants, Medicinal ; Sanguisorba ; Sodium* ; Succinic Acid* ; Superoxide Dismutase ; Triglycerides

OBJECTIVETo study the chemical components of essential oils from Meconopsis oliverana and their antioxidant activity.

METHODThe essential oil was extracted by steam distillation, and GC-MS analysis was used to identify its constituents. The OH free radical scavenging activity of the essential oils was evaluated with an enzyme mark instrument by assay of the ability of DPPH free radical scavenging. BHT was used as positive control.

RESULTForty-seven compounds, account for 91.866% of the essential oils, were identified. The ability of scavenging OH and DPPH radicals of the essential oils is stronger than that of BHT.

CONCLUSIONThe main chemical constituents of the essential oils from M. oliverana are n-hexadecanoic acid (27.653%) and 6,10,14-trimethyl-2-pentadecanone (16.330%). And the essential oils showed strong antioxidant activity.

Antioxidants ; chemistry ; metabolism ; Biphenyl Compounds ; metabolism ; Butylated Hydroxytoluene ; metabolism ; China ; Fatty Alcohols ; chemistry ; isolation & purification ; Free Radical Scavengers ; chemistry ; metabolism ; Gas Chromatography-Mass Spectrometry ; Hydroxyl Radical ; metabolism ; Oils, Volatile ; chemistry ; isolation & purification ; Oxidation-Reduction ; Palmitic Acid ; chemistry ; isolation & purification ; Papaveraceae ; chemistry ; Picrates ; metabolism ; Plant Oils ; chemistry ; isolation & purification

Oxidative stress plays a pivotal role in the pathogenesis of varied nervous system diseases. Recent studies have demonstrated that hydrogen has selective antioxidative effect. It selectively reduces the hydroxyl radical (*OH) and peroxynitrite (ONOO(-)), the most cytotoxic of reactive oxygen species (ROS); however, it does not affect other ROS, which play important physiological roles at low concentrations. A large body of experimental studies has proved that hydrogen, through anti-oxidation, anti-inflammatory and inhibiting apoptosis, has a significant therapeutic effect in various neurological diseases, such as ischemia, hypoxia, degeneration and spinal cord contusion. It provides us with a new clinical method for the prevention and treatment of neurological diseases.
Antioxidants ; pharmacology ; Humans ; Hydrogen ; pharmacology ; Hydroxyl Radical ; metabolism ; Nervous System ; drug effects ; metabolism ; Nervous System Diseases ; drug therapy ; metabolism ; Oxidative Stress ; drug effects ; physiology ; Peroxynitrous Acid ; metabolism

Animals ; Female ; Hydroxyl Radical ; metabolism ; Lipid Peroxidation ; physiology ; Liver ; metabolism ; Male ; Physical Conditioning, Animal ; physiology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sex Factors ; Time Factors

OBJECTIVETo investigate the correlation of perihematomal free radical level and neuronal apoptosis following the intracerebral hemorrhage (ICH).

METHODSAnimals were randomly divided into 4 groups: sham operation group, model group, 1 mg/kg edaravone group, and 3 mg/kg edaravone group. Each group was then divided into seven subgroups, in which the rats were correspondingly killed at 6 h, 12 h, 24 h, 48 h, 72 h, 7 d or 14 d (n = 1 in each subgroup of the sham group, and n = 6 in each subgroup of the other 3 groups). By Horseley-Clarke technique, autoblood (80 microL) were administered into the left caudate putamen of SD rats in a double administration-withdrawal way. Rats in the sham group were needled in but not administered with autoblood. The ICH model was then evaluated by Bederson's scale. Around the hematoma, the levels of malonaldehyde (MDA) and hydroxyl radical were tested by spectrophotometer, and the process of apoptosis was tested by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) method.

RESULTS(1) ICH significantly increased the levels of MDA and hydroxyl radicals. Significant differences in MDA and hydroxyl radical contents were observed among the four groups. (2) In the sham group, a small number of TUNEL-positive cells were found. In the other three groups, the TUNEL-positive cells were observed at 6 h, increased significantly at 24 h, and reached peak level at 3 d, then fell profoundly at 7 d, but remained detectable at 14 d. (3) The positive correlation existed between apoptosis and free radical level (r = 0.2003), and existed between apoptosis and MDA content (r = 0.6563) in the brain.

CONCLUSIONPost-hemorrhagic apoptosis was related to the production of free radicals, indicating that the elevated free radicals following the ICH could induce neuron and glial cell apoptosis.

Analysis of Variance ; Animals ; Antipyrine ; analogs & derivatives ; therapeutic use ; Apoptosis ; drug effects ; physiology ; Cerebral Hemorrhage ; drug therapy ; metabolism ; physiopathology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Free Radical Scavengers ; therapeutic use ; Hydroxyl Radical ; metabolism ; In Situ Nick-End Labeling ; methods ; Linear Models ; Male ; Malondialdehyde ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Time Factors

OBJECTIVEThe selective loss of dopaminergic neurons in Parkinson's disease is suspected to correlate with the increase of cellular iron, which may be involved in the pathogenesis of PD by promotion of oxidative stress. This research investigated dopamine-induced oxidative stress toxicity contributed by iron and the production of dopamine-derived neurotoxins in dopaminergic SH-SY5Y cells.

METHODSAfter the SH-SY5Y cells were pre-incubated with dopamine and Fe2+ for 24 h, the cell viability, hydroxyl radical, melondialdehyde, cell apoptosis, and catechol isoquinolines were measured by lactate dehydrogenase assay, salicylic acid trapping method, thiobarbuteric acid assay, Hoechst 33258 staining and HPLC-electrochemical detection (HPLC-ECD), respectively.

RESULTS(1) Optimal dopamine (150 micromol/L) and Fe2+ (40 or 80 micromol/L) significantly increased the concentrations of hydroxy radicals and melondialdehyde in SH-SY5Y cells. (2) Induction with dopamine alone or dopamine and Fe2+ (dopamine/Fe2+) caused cell apoptosis. (3) Compared with untreated cells, the catechol isoquinolines, salsolinol and N-methyl-salsolinol in dopamine/Fe2+-induced cells were detected in increasing amounts.

CONCLUSIONDue to dopamine/Fe2+-induced oxidative stress similar to the state in the parkinsonian substantia nigra neurons, dopamine and Fe2+ impaired SH-SY5Y cells could be used as the cell oxidative stress model of Parkinson's disease. The catechol isoquinolines detected in cells may be involved in the pathogenesis of Parkinson's disease as potential neurotoxins.

Apoptosis ; drug effects ; physiology ; Catechols ; metabolism ; Cell Line, Tumor ; Cell Survival ; drug effects ; physiology ; Dopamine ; toxicity ; Dose-Response Relationship, Drug ; Humans ; Hydroxyl Radical ; metabolism ; Iron ; metabolism ; Iron Metabolism Disorders ; complications ; metabolism ; physiopathology ; Isoquinolines ; metabolism ; Malondialdehyde ; metabolism ; Models, Biological ; Nerve Degeneration ; chemically induced ; metabolism ; physiopathology ; Neurons ; drug effects ; metabolism ; Neurotoxins ; toxicity ; Oxidative Stress ; drug effects ; Parkinson Disease ; etiology ; metabolism ; physiopathology ; Salsoline Alkaloids ; metabolism ; Up-Regulation ; drug effects ; physiology

Several studies have demonstrated that ischemic preconditioning increases superoxide dismutase activity, but it is unclear how ischemic preconditioning affects events downstream of hydrogen peroxide production during subsequent severe ischemia and reperfusion in the hippocampus. To answer this question, we investigated whether ischemic preconditioning in the hippocampal CA1 region increases the activities of antioxidant enzymes glutathione peroxidase and catalase, resulting in a decrease in the level of hydroxyl radicals during subsequent severe ischemia-reperfusion. Transient forebrain ischemia was induced by four-vessel occlusion in rats. Ischemic preconditioning for 3 min or a sham operation was performed and a 15-min severe ischemia was induced three days later. Ischemic preconditioning preserved the CA1 hippocampal neurons following severe ischemia. The concentration of 2,3-dihydroxybenzoic acid, an indicator of hydroxyl radical, was measured using in vivo microdialysis technique combined with HPLC. The ischemia-induced increase in the ratio of 2,3-dihydroxybenzoic acid concentration relative to baseline did not differ significantly between preconditioned and control groups. On the other hand, activities of the antioxidant enzymes glutathione peroxidase-1 and catalase were significantly increased at 3 days after ischemic preconditioning in the hippocampus. Our results suggest that, in preconditioned rats, while hydrogen peroxide is generated from severe ischemia, the activity of catalase and glutathione peroxidase-1 is correspondingly increased to eliminate the excessive hydrogen peroxide. However, our results show that the enhanced activity of these antioxidant enzymes in preconditioned rats is not sufficient to decrease hydroxyl radical levels during subsequent severe ischemia-reperfusion.
Animals ; Antioxidants/*metabolism ; Catalase/metabolism ; Enzyme Activation ; Glutathione Peroxidase/metabolism ; Hippocampus/*blood supply ; Hydrogen Peroxide/metabolism ; Hydroxybenzoic Acids/metabolism ; Hydroxyl Radical/*metabolism ; Ischemic Attack, Transient/*metabolism/physiopathology/prevention & control ; *Ischemic Preconditioning ; Male ; *Prosencephalon ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury/metabolism/prevention & control

OBJECTIVE: To explore the effect and possible mechanism of catechin microcapsulation on the repair of DNA damage in glumreular mesangial cells (GMCs) induced by H2O2. METHODS: According to H2O2 concentration, the experiment GMCs were divided into 6 groups: a control group, 50 micromol/L group, 100 micromol/L group, 150 micromol/L group, 200 micromol/L group and 250 micromol/L group. Each group was sub-divided into 3 groups: 6 h group, 12 h group and 24 h group, in order to determining the optimum dose and the best time of detecting the DNA damage in GMCs. The cultured cells were divided into 8 groups as follows: the NS control group, the H2O2 group, the catechin groups (the final concentrations were 10.0, 15.0, and 20.0 mg/L respectively) and the various catechin microcapsulation groups (the final concentrations were 10.0, 15.0, and 20.0 mg/L respectively). At the end of the experiment, hydroxy radical (OH), malonydialdehyde (MDA) and total superoxide dismutase (tSOD) concentration of supernadant in GMCs were determined by biochemistry assay, the repair of DNA damage in GMCs were detected by single cell gel electrophoresis assay. RESULTS: (1)At 6th h, H2O2 of 100 micromoL/L could cause the DNA damage of GMCs, and H2O2 of 150 micromol/L could result in DNA damage significantly. (2) No difference was found in the comet span of GMCs DNA in the catechin group and catechin microcapsulation group of different concentrations, while the DNA comet tail-long in the catechin microcapsulation group was shorter than that of the catechin group(all P(s)<0.05), and the fluorescence intensity of tail in the catechin microcapsulation group was lower than that of the catechin group(all P(s)<0.01). (3)When the concentration of catechin was 10.0 mg/L, no statistical significance was obtained in the concentration of dOH-, MDA and tSOD between the catechin microcapsulation group and the catechin group; while dOH- and MDA concentrations were lower, and the tSOD was higher in the catechin microcapsulation group than that in the catechin group when the concentration of catechin was 15.0 mg/L and 20.0 mg/L(all P(s)<0.05). CONCLUSION Catechin microcapsulation can enhance the GMCs ability of repairing DNA damage,which may be due to elevating the capacity of its anti-oxidation by catechin microcapsulation.
Animals ; Capsules ; Catechin ; pharmacology ; Cells, Cultured ; Comet Assay ; DNA Damage ; drug effects ; DNA Repair ; drug effects ; Dose-Response Relationship, Drug ; Hydrogen Peroxide ; toxicity ; Hydroxyl Radical ; metabolism ; Malondialdehyde ; metabolism ; Mesangial Cells ; drug effects ; metabolism ; pathology ; Rats ; Superoxide Dismutase ; metabolism

OBJECTIVETo investigate the effect and mechanism of prepared Radix Polygoni Multiflori (RPM) on the elevation of extracellular hydroxyl radical in striatum of rats induced by intracerebral perfusion of 6-hydroxy dopamine (6-OHDA).

METHODSCerebral microdialysis was used to establish the model. Hydroxyl radical was captured by salicylic acid, and 2,3-dihydroxy benzyl acid (2,3-DHBA) and 2,5-dihydroxy benzyl acid (2,5-DHBA) formed by hydroxyl radical in vital brain were measured by high performance liquid chromatography-electrochemical detector (HPLC-ED).

RESULTSAfter perfusion of 6-OHDA in brain of rats, the levels of 2,3-DHBA and 2,5-DHBA in the model group increased rapidly. The former was higher during the whole course of observation (P<0.01), while the latter was higher at most time points than that in the control group (P<0.05 or P<0.01). The level of 2,3-DHBA in the RPM group was lower than that in the model group at 5 time points (P < 0.05, P < 0. 01).

CONCLUSIONRPM could inhibit the elevating of extracellular hydroxyl radical in striatum of rats induced by intracerebral perfusion of 6-OHDA, indicating one of the brain protective mechanisms of RPM may be related to its anti-oxidation effect.

Animals ; Corpus Striatum ; drug effects ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Hydroxyl Radical ; metabolism ; Male ; Microdialysis ; Neuroprotective Agents ; pharmacology ; Oxidopamine ; Polygonum ; chemistry ; Random Allocation ; Rats ; Rats, Sprague-Dawley