OBJECTIVETo investigate the cytoprotective effects of Saeng-kankunbi-tang (, SKT), a herbal prescription consisting of Artemisia capillaris and Alisma canaliculatum, and its underlying mechanism involved.

METHODSIn mice, blood biochemistry and histopathology were assessed in carbon tetrachloride (CCl4)-induced oxidative hepatic injury in vivo. The animal groups included vehicle-treated control, CCl4, SKT 500 mg/(kg day) CCl4+SKT 200 or 500 mg/(kg day). In HepG2 cell, tert-butyl hydroperoxide (tBHP) induced severe oxidative stress and mitochondrial dysfunction in vitro. The cyto-protective effects of SKT were determined by 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay, flfluorescence activated cell sorting analysis and western blotting.

RESULTSThe administration of SKT prevented liver damage induced by CCl4 in mice, by inhibition of hepatocyte degeneration and inflflammatory cell infifiltration as well as plasma parameters such as alanine aminotransferase (P<0.01). Moreover, treatment with tBHP induced hepatocyte death and cellular reactive oxygen species production in hepatocyte cell line. However, SKT pretreatment (30-300 μg/mL) reduced this cell death and oxidative stress (P<0.01). More importantly, SKT inhibited the ability of tBHP to induce changes in mitochondrial membrane transition in cell stained with rhodamine 123 P<0.01). Furthermore, treatment with SKT induced extracellular signal-regulated kinases-mediated nuclear factor erythroid-2-related factor 2 (Nrf2) activation as well as the expressions of heme oxygenase 1 and glutamate- cystein ligase catalytic, Nrf2 target genes.

CONCLUSIONSSKT has the ability to protect hepatocyte against oxidative stress and mitochondrial damage mediated by Nrf2 activation.

Animals ; Antioxidants ; pharmacology ; Carbon Tetrachloride ; Cell Death ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Hep G2 Cells ; Humans ; Liver ; drug effects ; enzymology ; pathology ; MAP Kinase Signaling System ; drug effects ; Mice, Inbred C57BL ; Mitochondria ; drug effects ; metabolism ; NF-E2-Related Factor 2 ; metabolism ; Oxidative Stress ; drug effects ; Peroxides ; Phosphorylation ; drug effects ; Protective Agents ; pharmacology ; Reactive Oxygen Species ; metabolism

OBJECTIVETo investigate the acting mechanism of Buxu Huayu Qutan Decoction (BHQD) for impacting the anti-oxidative capacity in aged patients with stable angina pectoris of coronary heart disease (AP-CHD).

METHODSForty patients of AP-CHD, Chinese medicine diagnosed as Xiong-bi, were equally assigned to the treatment group and the control group. Superoxide dismutase (SOD) activity and lipid peroxide (LPO) contents in blood, and mRNA expression of manganese-containing superoxide dismutase (MnSOD) in peripheral mononuclear cells were determined before and after treatment by biochemical and molecular biologic techniques.

RESULTSNo significant change of plasma SOD and LPO was found in the control group after treatment (P >0.05), while the plasma SOD activity increased and LPO content lowered in the treatment group significantly (P<0.01). Moreover, mRNA expression of MnSOD in the treatment group after treatment was obviously higher than that in the control group (P <0.01).

CONCLUSIONSThe acting mechanism of BHQD for AP-CHD treatment might partially due to its effects in inducing gene expression of MnSOD in mononuclear cells, enhancing SOD activity, decreasing LPO content, maintaining oxidation/antioxidation equilibrium in myocardial cells, blocking the chain reaction of lipid peroxidation, intervening the production and enhancing the scavenging of oxygen free radicals.

Aged ; Angina Pectoris ; drug therapy ; metabolism ; Coronary Disease ; drug therapy ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Female ; Humans ; Lipid Peroxidation ; Lipid Peroxides ; blood ; Male ; Middle Aged ; Oxidative Stress ; Phytotherapy ; Superoxide Dismutase ; metabolism

This study was performed to investigate the effect of chongkukjang intake on lipid metabolism and liver function in ethanol consumed rats. Twenty one Sprague-Dawley male rats aging 4 weeks old were used as experimental animals, which were divided into three dietary groups: casein diet (CA), soybean diet (SB) and chongkukjang diet (CJ). Alcohol was consumed with water as 25% (v/v) ethanol solution. After 4 weeks of experimental period, rats were sacrificed to get blood and liver samples for analysis of lipids, lipid peroxides, antioxidative enzymes and biochemical indices of liver function. The mean body weight, food intake and liver index were not significantly different among three groups. Serum level of total lipid, triglyceride and total cholesterol of chongkukjang diet group was the lowest among three groups although the difference was not significant. HDL-cholesterol level was significantly (p < 0.05) higher in chongkukjang diet group than that of casein diet group. LDL-cholesterol level of chongkukjang and soybean diet group was significantly (p < 0.05) lower than that of casein diet group respectively. Liver TBARS of chongkukjang and soybean diet group was significantly (p < 0.05) lower than that of casein diet group respectively. The superoxide dismutase activity of chongkukjang diet group was significantly (p < 0.05) higher than that of casein diet group. Catalase activity was not significantly different among three groups. As indices of liver function, glutamic oxaloacetic transminase (GOT), glutamic pyruvic transminase (GPT), gamma-glutamyl transpeptidase (gamma-GTP) and lactate dehydrogenase (LDH) were not significantly different among three groups. Serum alcohol concentration and activities of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) were not significantly different among three groups. The chongkukjang diet seems to give a beneficial effect for improving lipid metabolism by increasing HDLcholesterol level and SOD activity while reducing liver TBARS level. However, effect on liver function has to be investigated further.
Aging ; Alcohol Dehydrogenase ; Aldehyde Dehydrogenase ; Animals ; Body Weight ; Caseins ; Catalase ; Cholesterol ; Diet ; Eating ; Ethanol* ; gamma-Glutamyltransferase ; Humans ; L-Lactate Dehydrogenase ; Lipid Metabolism* ; Lipid Peroxides ; Liver* ; Male ; Rats* ; Rats, Sprague-Dawley ; Soybeans ; Superoxide Dismutase ; Thiobarbituric Acid Reactive Substances ; Triglycerides ; Water

OBJECTIVETo examine changes of blood oxidative-antiovidative level in schizophrenic patients and its relationship with clinical symptoms.

METHODSForty-six Chinese patients met DSM-IV (Diagnostic and Statistical Manual of Mental Disorders-IV) criteria for schizophrenia and fifty age- and sex-matched healthy controls were enrolled in the present study. Baseline psychiatric symptom severity was assessed with brief psychiatric rating scale, positive and negative syndrome scale on the blood draw day. Fresh blood samples were collected to measure levels of nitric oxide and lipid peroxide in plasma as well as activities of superoxide dismutase, catalase and glutathione peroxidase in red blood cells by spectrophotometric assays simultaneously.

RESULTSComparison of the biochemical parameters indicated that the level of nitric oxide and lipid peroxide increased in patient group, which represented a positive correlation with positive scale scores; while the activities of three critical enzymes decreased and showed a negative linear correlation.

CONCLUSIONThis study showed that there are dysregulation of free radical metabolism and poor activities of the antioxidant defense systems in schizophrenic patients. Excess free radicals formation may play a critical role in the etiology of schizophrenia. Using antioxidants might be an effective therapeutic approach to partially alleviate or prevent the symptoms of schizophrenia.

Adolescent ; Adult ; Antioxidants ; metabolism ; Female ; Free Radicals ; Humans ; Lipid Peroxides ; metabolism ; Male ; Middle Aged ; Nitric Oxide ; metabolism ; Schizophrenia ; etiology ; metabolism

OBJECTIVETo observe clinical therapeutic effect of head point-through-point electroacupuncture on Parkinson's disease and the mechanism.

METHODSSeventy-six cases of Parkinson's disease were randomly divided into a treatment group (n=37) treated with head point-through-point electroacupuncture and oral administration of madopa, and a control group (n=39) with only oral administration of madopa. Superoxide dismutase (SOD) and lipids peroxides (LPO) were determined before and after treatment.

RESULTSThe effective rate was 97.3% in the treatment group and 61.5% in the control group with a very significant difference between the two groups (P < 0.01). SOD activity and LPO content were significantly improved after treatment in the treatment group (P < 0.01), with a significant difference between the two groups (P < 0.01).

CONCLUSIONHead point-through-point electroacupuncture can improve SOD activity and LPO content in the body so as to cure Parkinson's disease.

Acupuncture Points ; Adult ; Aged ; Electroacupuncture ; methods ; Female ; Head ; Humans ; Lipid Peroxides ; analysis ; Male ; Middle Aged ; Parkinson Disease ; metabolism ; therapy ; Superoxide Dismutase ; metabolism

Heme oxygenase-1 (HO-1) has been described as an inducible protein that is capable of cytoprotection via radical scavenging and the prevention of apoptosis. Chronic exposure to hyperglycemia can lead to cellular dysfunction that may become irreversible over time, and this process has been termed glucose toxicity. Yet little is known about the relation between glucose toxicity and HO-1 in the islets. The purposes of the present study were to determine whether prolonged exposure of pancreatic islets to a supraphysiologic glucose concentration disrupts the intracellular balance between reactive oxygen species (ROS) and HO-1, and so this causes defective insulin secretion; we also wanted to evaluate a protective role for HO-1 in pancreatic islets against high glucose levels. The intracellular peroxide levels of the pancreatic islets (INS-1 cell, rat islet) were increased in the high glucose media (30 mM glucose or 50 mM ribose). The HO-1 expression was induced in the INS-1 cells by the high glucose levels. Both the HO-1 expression and glucose stimulated insulin secretion (GSIS) was decreased simultaneously in the islets by treatment of the HO-1 antisense. The HO-1 was upregulated in the INS-1 cells by hemin, an inducer of HO-1. And, HO-1 upregulation induced by hemin reversed the GSIS in the islets at a high glucose condition. These results suggest HO-1 seems to mediate the protective response of pancreatic islets against the oxidative stress that is due to high glucose conditions.
Reactive Oxygen Species ; Rats, Wistar ; Rats ; Peroxides/metabolism ; Oxidative Stress ; Male ; Islets of Langerhans/*metabolism ; Insulin/secretion ; Hemin/metabolism ; Heme Oxygenase-1/metabolism/*physiology ; Glucose/metabolism/*pharmacology ; *Gene Expression Regulation ; Flow Cytometry ; Animals

OBJECTIVETo investigate the effect of N-acetyl-cysteine (NAC) and depakine (DP) on the changes of membrane potential and peroxidate in rat cortex neurons exposed to ferrous chloride (FeCl(2)).

METHODSCultured cortex neurons of newly born SD rats were randomly divided into control group (PBS group), model group (FeCl(2) group), NAC pretreatment group (NAC group), DP pretreatment group (DP group) and NAC+DP pretreatment group (NAC+DP group). In the latter three groups, NAC (0.08 mg/ml) and DP (0.1 mg/ml) were added in the cell culture 2 and 3 h before FeCl(2) (1 mmol/L) exposure, respectively. After exposure to FeCl(2), the membrane potential of the neurons was detected with fluorescent dye DiBAC4(3) (bis-(1,3-dibutylbarbituric acid) trimethine oxonol), and the peroxidate level with 2,7-dichlorofluorescin diacetate (H(2)DCF) by laser confocal scanning microscope (LCSM) and nuclear factor-KappaB (NF-KappaB) level with immunocytochemistry.

RESULTSCompared with FeCl(2) group, the expression of NF-KappaB and peroxidate level in the neurons were decreased significantly in NAC and NAC+DP groups (P<0.01), but not in DP group (P>0.05). FeCl(2) depolarized the membrane potential and increased the expression of NF-KappaB in the neurons. Compared with FeCl(2) group, significant changes in the membrane potential were observed in DP and NAC+DP groups (P<0.01) but not in NAC or PBS group (P>0.05).

CONCLUSIONBoth NAC and DP can protect the neurons from FeCl(2)-induced damage but through different pathways, and their combined use can significantly alleviate neuronal damages due to FeCl(2) exposure. Antioxidants such as NAC in combination with antiepileptic drugs may produce favorable effect in prevention and treatment of posttraumatic epilepsy.

Acetylcysteine ; pharmacology ; Animals ; Animals, Newborn ; Cells, Cultured ; Cerebral Cortex ; cytology ; metabolism ; physiopathology ; Female ; Ferrous Compounds ; pharmacology ; Male ; Membrane Potentials ; drug effects ; Neurons ; cytology ; metabolism ; physiology ; Neuroprotective Agents ; pharmacology ; Peroxides ; metabolism ; Rats ; Rats, Sprague-Dawley ; Valproic Acid ; pharmacology

OBJECTIVETo study the therapeutic effects and mechanism of Jiechangning (JCN) decoction on carrageenan induced experimental ulcerative colitis (UC).

METHODSAfter sensitizing guinea pigs with carrageenan, we established UC animal models by free drinking water containing 2% acid degraded carrageenan (ADC). JCN decoction was orally administered once a day for 2 weeks after carrageenan treatment. Salicylazosulfapyridine (SASP) and normal saline were given to the other two groups as control. The levels of colon lipid peroxide (LPO), acid phosphatase (ACP) activity and tumor necrosis factor-alpha (TNF-alpha) were measured; colitis activity score (CAS) was carried out for assessment of the degree of tissue inflammation and injury; the colonic pathological changes were examined simultaneously with hematoxylin and eosin (HE) and toluidine blue staining used to evaluate the therapeutic effects of JCN decoction and SASP.

RESULTSExperimental colitis models resembling human UC were successfully induced. The levels of tissue LPO, ACP activity and the content of tissue TNF-alpha were markedly increased in the model group as compared with the normal control group (P < 0.01) and were positively correlated with CAS. JCN decoction could reverse these changes like SASP. HE staining showed that JCN decoction and SASP could reduce CAS and the degree of tissue injury, toluidine blue staining revealed that mucosa and submucosa red metachromasia pellets in JCN group and SASP group were markedly fewer than those in the model group.

CONCLUSIONJCN decoction is effective in treating experimental UC, which provides theoretical basis for its clinical application.

Acid Phosphatase ; metabolism ; Animals ; Carrageenan ; Colitis, Ulcerative ; chemically induced ; metabolism ; pathology ; Colon ; drug effects ; metabolism ; pathology ; Gastrointestinal Agents ; pharmacology ; Guinea Pigs ; Lipid Peroxides ; metabolism ; Male ; Medicine, Chinese Traditional ; Plant Preparations ; pharmacology ; Sulfasalazine ; pharmacology ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo observe the analgesic effect of Zhitong Capsule (ZTC) and study its mechanism in adjuvant arthritis (AA) rats.

METHODSForty-eight male Sprague-Dawley rats were randomly divided into six groups with 8 rats in each group. On the first day, except to those in the normal group that were treated with normal saline, the same amount of Freund's complete adjuvant (FCA) was given through intradermal injection into the right hind paw to all the rats in the other groups. From the 17th day of the modeling on, the rats in groups of ZTC were administered daily through gastrogavage with a dose of 1000, 500, 250 mg/kg respectively, while equal volume of normal saline was given to those in the normal group and model group, and an equal volume of aspirin (ASA) solution was given to rats in the ASA group through gastrogavage for 10 days, once per day, and on the 27th day, the analgesic effect of ZTC was measured with heat withdraw method. The activities and contents of superoxide dismutase (SOD) and lipid peroxides (LPO) in serum were observed by spectrophotometry, and the level of beta-endorphin (beta-EP) in hypothalamus were determined by the assay of immunohistochemistry.

RESULTSZTC showed significant effects on enhancing the pain threshold and at the same time it increased the activities of SOD and reduced the contents of LPO in serum. ZTC could also increase the level of beta-EP in hypothalamus.

CONCLUSIONZTC has analgesic effect and its mechanism is probably related with its effect in inhibiting the level of oxygen free radicals in serum and increasing the level of beta-EP of hypothalamus in rats.

Analgesia ; methods ; Animals ; Arthritis, Experimental ; metabolism ; physiopathology ; therapy ; Hypothalamus ; metabolism ; Lipid Peroxides ; blood ; Male ; Medicine, Chinese Traditional ; Pain ; physiopathology ; Pain Threshold ; drug effects ; Phytotherapy ; Plant Preparations ; therapeutic use ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; blood ; Tissue Distribution ; beta-Endorphin ; metabolism

OBJECTIVETo discuss the protective effects of pueraria compound on the cerebral ischemic injury.

METHODUsing the middle cerebral artery occlusion model (MCAO) in rats and cerebral ischemia-reperfusion models in gerbils and mice, we investigated the influence of pueraria compound on the brain water content and the infarct size, the cerebral apoplexy exponent, the contents of lactic acid (LA) and lipid peroxide (LPO), the activities of lactic dehydrogenase (LDH), glutathione peroxidase (GPx) and Na+ -K+ -ATPase.

RESULTPueraria compound obviously reduced the brain water content and the infrarct size in MCAO, improved motor abilities in the cerebral ischemia-reinfusion model of gerbils, decreased the contents of LA and LPO and increased the activities of LDH, GPx and Na+ -K+ -ATPase in cerebral ischemia-reinfusion model of mice.

CONCLUSIONPueraria compound has the function of antioxidation and protective effect on ischemic brain tissue.

Animals ; Antioxidants ; isolation & purification ; pharmacology ; Brain ; metabolism ; pathology ; Brain Ischemia ; metabolism ; pathology ; Drug Combinations ; Gerbillinae ; Glutathione Peroxidase ; metabolism ; Isoflavones ; isolation & purification ; pharmacology ; L-Lactate Dehydrogenase ; metabolism ; Lactic Acid ; metabolism ; Lipid Peroxides ; metabolism ; Male ; Mice ; Neuroprotective Agents ; isolation & purification ; pharmacology ; Plants, Medicinal ; chemistry ; Pueraria ; chemistry ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; pathology ; Sodium-Potassium-Exchanging ATPase ; metabolism ; Soybeans ; chemistry