Objective: This study aimed to investigate the effect of exposure to a 900 MHz electromagnetic field (EMF) on the cervical spinal cord (CSC) of rats and the possible protective effect of luteolin (LUT) against CSC tissue damage. Methods: Quantitative data were obtained stereological, biochemical, immunohistochemical, and histopathological techniques. We investigated morphometric value, superoxide dismutase (SOD) level, and the expression of high-mobility group box 1 protein molecules, as well as histological changes. Results: The total number of motor neurons in the EMF group significantly decreased in comparison with that in the control group ( < 0.05). In the EMF + LUT group, we found a significant increase in the total number of motor neurons compared with that in the EMF group ( < 0.05). SOD enzyme activity in the EMF group significantly increased in comparison with that in the control group ( < 0.05). By contrast, the EMF+LUT group exhibited a decrease in SOD level compared with the EMF group ( < 0.05). Conclusion Our results suggested that exposure to EMF could be deleterious to CSC tissues. Furthermore, the protective efficacy of LUT against SC damage might have resulted from the alleviation of oxidative stress caused by EMF.
Animals ; Antioxidants ; pharmacology ; Electromagnetic Fields ; adverse effects ; Luteolin ; pharmacology ; Male ; Rats ; Rats, Wistar ; Spinal Cord ; drug effects ; radiation effects

Oxidative stress and lipid peroxidation have been implicated in the pathogenesis of various diseases, including atherosclerosis and fatty liver diseases, and consequently the role of antioxidants in the prevention and treatment of such diseases has received much attention. In particular, the effects of vitamin E, the most important lipophilic radical-scavenging antioxidant, have been investigated extensively. Many in vitro, animal, and epidemiological studies have reported positive results, but large-scale randomized controlled intervention studies and meta-analyses have produced inconsistent and often disappointing results. In the present review article, the role and action of vitamin E are discussed, with consideration of the factors that determine the outcome of vitamin E treatment. Vitamin E should benefit subjects experiencing oxidative stress due to free radicals when administered at the correct time and for an appropriate duration.
Animals ; Antioxidants/adverse effects/*therapeutic use ; Humans ; Lipid Peroxidation/*drug effects ; Oxidative Stress/*drug effects ; Reactive Oxygen Species/*metabolism ; Vitamin E/adverse effects/*therapeutic use

Alzheimer's disease (AD) has become one of the most important and most interesting focuses in the field of medical and scientific research. Up to now, the pathogenesis of AD has not been completely clarified. However, the high-density of amyloid β-protein (Aβ) in senile plaques of AD brain and the neurotoxicity of Aβ have been indisputable facts. The mechanisms underlying Aβ neurotoxicity are very complicated, involving calcium overload, inflammation, ion channel dysfunction, oxidative stress and so on. Among all of those, the mechanism of oxidative stress in Aβ neurotoxicity and the experimental progress of antioxidants in AD treatment have been widely reported in recent years. This review mainly discussed current research progresses on the oxidative stress of Aβ, so as to provide readers with some clues to the antioxidant therapy of AD.
Alzheimer Disease ; etiology ; metabolism ; physiopathology ; Amyloid beta-Peptides ; adverse effects ; metabolism ; Animals ; Antioxidants ; pharmacology ; Humans ; Oxidative Stress ; drug effects ; physiology

The objective of this study was to investigate the protection by naringenin against doxorubicin-induced oxidative damage in normal blood cells. Inhibiting effects of naringenin, doxorubicin and naringenin combined with doxorubicind on K562 cells and polymorphonuclear leukocytes were detected with MTT method, the level of reactive oxygen species (ROS) and lipid peroxidation (MDA), the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were examined with spectrophotometric method in the K562 cells and polymorphonuclear leukocytes. The results indicated that the proliferation of K562 cells was not inhibited by the cytotoxicity of doxorubicin in combination of naringenin with doxorubicin. As compared with the doxorubicin, the addition of naringenin after doxorubicin for 1 hour, the levels of reactive oxygen species (ROS) and lipid peroxidation (MDA) obviously decreased, the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) obviously increased in the polymorphonuclear leukocytes, but these were not changed obviously in K562 cells. It is concluded naringenin can protect against doxorubicin-induced oxidative damage in normal blood cells. The mechanism of naringenin may be elevating activities of antioxidant enzyme and degrading oxidative production level in normal blood cells, and meanswhile decreasing level of oxidative products.
Antioxidants ; pharmacology ; Doxorubicin ; adverse effects ; Erythrocytes ; drug effects ; Flavanones ; pharmacology ; Humans ; Oxidative Stress ; Reactive Oxygen Species ; metabolism ; Superoxide Dismutase ; metabolism

AIMTo investigate the preventive effects of Panax notoginseng saponins (PNS) and Ginkgo biloba extracts (GbE) on acute oxygen toxicity and the possible mechanisms.

METHODSMice were injected intraperitoneally with PNS and GbE for 5 days, then were exposed to 500 kPa hyperbaric oxygen (HBO) for 60 min, the convulsion latency, times and interval were observed. Moreover, reactive oxygen (RO) unit, MDA, NO, GSH levels and GSH-Px, CAT, MAO activities of mice brain were determined after they were exposed to HBO for 15 min.

RESULTSPNS and GbE could markedly prolong the convulsion latency and interval, reduce convulsion times, decrease contents of MDA and NO in mice brain, keep RO unit, GSH and GSH-Px at higher levels, but had no effects on CAT and MAO activities.

CONCLUSIONPNS and GbE could effectively prevent acute oxygen toxicity, which were related to their antioxidant activities.

Animals ; Antioxidants ; pharmacology ; Diving ; adverse effects ; Ginkgo biloba ; Hyperbaric Oxygenation ; adverse effects ; Male ; Mice ; Oxygen ; poisoning ; Panax notoginseng ; Phytotherapy ; Plant Extracts ; pharmacology ; Saponins ; pharmacology

OBJECTIVE: To investigate the spectrum-effect relationship between the total anthraquinone extract of Cassia seeds and fluorouracil (5-Fu)-induced liver injury in mice and identify the effective components in the extract. METHODS: A mouse model of liver injury was established by intraperitoneal injection of 5-Fu, with bifendate as the positive control. The serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and myeloperoxidase (MPO), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) in the liver tissue were detected to investigate the effect of the total anthraquinone extract of Cassia seeds (0.4, 0.8 and 1.6 g/kg) on liver injury induced by 5-Fu. HPLC fingerprints of 10 batches of the total anthraquinone extracts were established to analyze the spectrum- effectiveness of the extract against 5- Fu- induced liver injury in mice and screen the effective components using the grey correlation method. RESULTS: The 5- Fu- treated mice showed significant differences in liver function parameters from the normal control mice (P < 0.05), suggesting successful modelling. Compared with those in the model group, serum ALT and AST activities were decreased, SOD and T- AOC activities significantly increased, and MPO level was significantly lowered in the mice treated with the total anthraquinone extract (all P < 0.05). HPLC fingerprints of the 31 components in the total anthraquinone extract of Cassia seeds showed good correlations with the potency index of 5-Fu-induced liver injury but with varying correlation strengths. The top 15 components with known correlations included aurantio-obtusina (peak 6), rhein (peak 11), emodin (peak 22), chrysophanol (peak 29) and physcion (peak 30). CONCLUSION The effective components in the total anthraquinone extract of Cassia seeds, including aurantio-obtusina, rhein, emodin, chrysophanol, and physcion, are coordinated to produce protective effects against 5-Fu-induced liver injury in mice.
Animals ; Mice ; Emodin ; Cassia ; Chemical and Drug Induced Liver Injury, Chronic ; Anthraquinones ; Antioxidants ; Fluorouracil/adverse effects* ; Plant Extracts/pharmacology*

OBJECTIVETo study the effects of extremely low frequency electromagnetic field(ELF EMF) and its combination with lead on the antioxidant system in mouse brain and liver tissues.

METHODMice were exposed to a 50 Hz sinusoidal 0.2 mT or 6.0 mT EMF for 2 weeks. At the same time, some groups were exposed to lead(50 mg/kg). After the exposure, the antioxidant system and cell membrane fluidity in brain and liver were measured.

RESULTSMalondiadehyde(MDA) content in brain and liver increased from the control levels of (1.33 +/- 0.12) and (3.95 +/- 0.21) nmol/mg pro to (1.35 +/- 0.09) and (6.15 +/- 0.28) nmol/mg pro respectively following 0.2 mT exposure, and to (3.98 +/- 0.10) and (6.50 +/- 0.79) nmol/mg pro respectively following 6.0 mT exposure. Total antioxidant capability(T-AOC) in brain and liver decreased from the control levels of (4.39 +/- 0.48) and (2.45 +/- 0.21) U/mg pro to (3.99 +/- 0.39) and (1.92 +/- 0.32) U/mg pro respectively following 0.2 mT, and to (3.12 +/- 0.37) and (1.57 +/- 0.14) U/mg pro respectively following 6.0 mT. GSH content decreased only in liver tissue from the control level of (194.60 +/- 20.93) mg/g pro to (189.24 +/- 5.61) mg/g pro(0.2 mT) and (153.04 +/- 1.18) mg/g pro(6.0 mT). Cellular membrane fluidity decreased from the control levels of (1.396 +/- 0.040) and (2.899 +/- 0.552) to (1.224 +/- 0.190) and (1.894 +/- 0.0761) (0.2 mT), (1.159 +/- 0.179) and (1.516 +/- 0.204)(6.0 mT) respectively. Compared with single EMF exposure(6.0 mT), EMF combined with lead exposure induced remarkable increase in MDA, GSH content and T-AOC and decrease in cell membrane fluidity both in the brain and liver, and increase in SOD activity only in liver.

CONCLUSIONELF EMF might alter the metabolism of free radicals, decrease anti-oxidant capability and enhance lipid peroxidation. The combination of EMF with lead showed synergic effects on lipid peroxidation.

Animals ; Antioxidants ; metabolism ; Brain ; drug effects ; metabolism ; radiation effects ; Electromagnetic Fields ; adverse effects ; Glutathione ; analysis ; Lead ; toxicity ; Lipid Peroxidation ; drug effects ; radiation effects ; Liver ; drug effects ; metabolism ; radiation effects ; Membrane Fluidity ; drug effects ; radiation effects ; Mice ; Superoxide Dismutase ; metabolism

Antioxidants ; pharmacology ; Ascorbic Acid ; pharmacology ; Carbon Disulfide ; adverse effects ; antagonists & inhibitors ; Cells, Cultured ; Endothelium, Vascular ; drug effects ; Humans ; Umbilical Veins ; cytology ; drug effects ; metabolism

A hyperuricemic rat model induced by adenine and ethambutol was established to investigate the anti-hyperuricemia activity and its mechanism of the flavonoid extract from saffron floral bio-residues. Sixty-seven SD rats were randomly divided into control group, model group, positive control group, and flavonoid extract groups(with 3 doses), respectively, and each group contained 11 or 12 rats. The hyperuricemic model was established by continuous oral administration of adenine(100 mg·kg~(-1)) and ethambutol(250 mg·kg~(-1)) for 7 days. At the same time, the positive control group was given allopurinol(20 mg·kg~(-1) per day) and the flavonoid extract groups were given the flavonoid extract at doses of 340, 170 and 85 mg·kg~(-1) per day, respectively. On day 8, rat serum, liver, kidney, and intestinal tissues were collected, and the levels of uric acid in serum and tissue, the xanthine oxidase activities and antioxi-dant activities in serum and liver were evaluated, and the kidney histopathology was explored. In addition, an untargeted serum metabolomics study was performed. According to the results, the flavonoid extract effectively reduced the uric acid levels in serum, kidney and ileum and inhibited the xanthine oxidase activities and elevated the antioxidant activities of serum and liver in hyperuricemic rat. At the same time, it reduced the levels of inflammation factors in kidney and protected renal function. Moreover, 68 differential metabolites of hyperuricemic rats were screened and most of which were lipids and amino acids. The flavonoid extract significantly retrieved the levels of differential metabolites in hyperuricemic rats, such as SM(d18:1/20:0), PC[18:0/18:2(92,12Z)], palmitic acid and citrulline, possibly through the following three pathways, i.e., arginine biosynthesis, glycine, serine and threonine metabolism, and histidine metabolism. To sum up, the flavonoid extract of saffron floral bio-residues lowered the uric acid level, increased the antioxidant activity, and alleviated inflammatory symptoms of hyperuricemic rats, which may be related to its inhibition of xanthine oxidase activity and regulation of serum lipids and amino acids metabolism.
Rats ; Animals ; Flavonoids/pharmacology* ; Uric Acid ; Crocus ; Xanthine Oxidase ; Ethambutol/adverse effects* ; Rats, Sprague-Dawley ; Hyperuricemia/drug therapy* ; Kidney ; Antioxidants/pharmacology* ; Plant Extracts/adverse effects* ; Amino Acids ; Adenine/adverse effects* ; Lipids

OBJECTIVE: To quantify phytochemicals using liquid chromatography and mass spectroscopy (LCMS) analysis and explore the therapeutic effect of Aesculus hippocastanum L. (AH) seeds ethanolic extract against gastric ulcers in rats. METHODS: Preliminary phytochemical testing and LCMS analysis were performed according to standard methods. For treatment, the animals were divided into 7 groups including normal control, ulcer control, self-healing, AH seeds low and high doses, ranitidine and per se groups. Rats were orally administered with 10 mg/kg of indomethacin, excluding the normal control group (which received 1% carboxy methyl cellulose) and the per se group (received 200 mg/kg AH seeds extract). The test group rats were then given 2 doses of AH seeds extract (100 and 200 mg/kg, respectively), while the standard group was given ranitidine (50 mg/kg). On the 11th day, rats in all groups were sacrificed, and their stomach was isolated to calculate the ulcer index, and other parameters such as blood prostaglandin (PGE₂), tissue superoxide dismutase (SOD), catalase (CAT), malonyldialdehyde (MDA), and glutathione (GSH). All isolated stomach tissues were analyzed for histopathological findings. RESULTS: The phytochemical examination shows that the AH seeds contain alkaloids, flavonoids, saponins, phenolic components, and glycosides. LCMS analysis confirms the presence of quercetin and rutin. The AH seeds extract showed significant improvement in gastric mucosa conditions after indomethacin-induced gastric lesions (P<0.01). Further marked improvement in blood PGE₂ and antioxidant enzymes, SOD, CAT, MDA and GSH, were observed compared with self-healing and untreated ulcer-induced groups (P<0.01). Histopathology results confirmed that AH seeds extract improved the mucosal layer and gastric epithelial membrane in treated groups compared to untreated ulcer-induced groups. CONCLUSIONS LCMS report confirms the presence of quercetin and rutin in AH seeds ethanolic extract. The therapeutic effect of AH seeds extract against indomethacin-induced ulcer in rat model indicated the regenerated membrane integrity, with improved cellular functions and mucus thickness. Further, improved antioxidant enzyme level would help to reduce PGE₂ biosynthesis.
Rats ; Animals ; Stomach Ulcer/pathology* ; Antioxidants/therapeutic use* ; Ranitidine/adverse effects* ; Aesculus ; Ulcer/drug therapy* ; Quercetin ; Plant Extracts/chemistry* ; Indomethacin/therapeutic use* ; Glutathione ; Superoxide Dismutase ; Rutin/adverse effects* ; Prostaglandins/adverse effects* ; Phytochemicals/therapeutic use*