scholarly journals Dose-Dependent Behavioral and Antioxidant Effects of Quercetin and Methanolic and Acetonic Extracts from Heterotheca inuloides on Several Rat Tissues following Kainic Acid-Induced Status Epilepticus

2019 ◽  
Vol 2019 ◽  
pp. 1-17
Author(s):  
Liliana Carmona-Aparicio ◽  
Noemí Cárdenas-Rodríguez ◽  
Guillermo Delgado-Lamas ◽  
José Pedraza-Chaverri ◽  
Hortencia Montesinos-Correa ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Status Epilepticus ◽  
Kainic Acid ◽  
Neuronal Damage ◽  
Brain Regions ◽  
Control Group ◽  
Rat Tissues ◽  
Protective Effects ◽  
Organic Extracts ◽  
Dose Dependent

Kainic acid (KA) has been used to study the neurotoxicity induced after status epilepticus (SE) due to activation of excitatory amino acids with neuronal damage. Medicinal plants can protect against damage caused by KA-induced SE; in particular, organic extracts of Heterotheca inuloides and its metabolite quercetin display antioxidant activity and act as hepatoprotective agents. However, it is unknown whether these properties can protect against the hyperexcitability underlying the damage caused by KA-induced SE. Our aim was to study the protective effects (with regard to behavior and antioxidant activity) of administration of natural products methanolic (ME) and acetonic (AE) extracts and quercetin (Q) from H. inuloides at doses of 30 mg/kg (ME30, AE30, and Q30 groups), 100 mg/kg (ME100, AE100, and Q100 groups), and 300 mg/kg (ME300, AE300, and Q300 groups) against damage in brain regions of male Wistar rats treated with KA. We found dose-dependent effects on behavioral and biochemical studies in the all-natural product groups vs. the control group, with decreases in seizure severity (Racine’s scale) and increases in seizure latency (p<0.05 in the ME100, AE100, Q100, and Q300 groups and p<0.01 in the AE300 and ME300 groups); on lipid peroxidation and carbonylated proteins in all brain tissues (p<0.0001); and on GPx, GR, CAT, and SOD activities with all the treatments vs. KA (p≤0.001). In addition, there were strong negative correlations between carbonyl levels and latency in the group treated with KA and in the group treated with methanolic extract in the presence of KA (r=‐0.9919, p=0.0084). This evidence suggests that organic extracts and quercetin from H. inuloides exert anticonvulsant effects via direct scavenging of reactive oxygen species (ROS) and modulation of antioxidant enzyme activity.

scholarly journals Effects of Propentofylline on Hypoxia—Hypoglycemia-Induced Calcium Accumulation in Gerbil Hippocampal Slices

1992 ◽  
Vol 12 (2) ◽  
pp. 301-305 ◽  
Author(s):  
Fumito Kadoya ◽  
Akira Mitani ◽  
Tatsuru Arai ◽  
Kiyoshi Kataoka
Keyword(s):  
Cerebral Ischemia ◽  
Intracellular Calcium ◽  
Neuronal Damage ◽  
Hippocampal Slices ◽  
Dependent Manner ◽  
Protective Effects ◽  
Calcium Accumulation ◽  
Xanthine Derivative ◽  
Acute Increase ◽  
Dose Dependent

The xanthine derivative propentofylline (HWA 285) has been reported to show protective effects against neuronal damage induced by cerebral ischemia. In the present study, microfluorometry was used to investigate the effect of propentofylline on the hypoxia–hypoglycemia-induced intracellular calcium accumulation in gerbil hippocampal slices. When slices were superfused with hypoxic–hypoglycemic medium that did not contain propentofylline, an acute increase in calcium accumulation was detected 75–200 s (mean latency of 123 s) after the beginning of hypoxia–hypoglycemia. When slices were superfused with hypoxic–hypoglycemic mediums that contained 10 μ M, 100 μ M, and 1 m M propentofylline, the latency of the acute increase in calcium accumulation was prolonged in all subregions of the hippocampus in a dose-dependent manner: mean latencies in field CA1 were 146, 168, and 197 s after hypoxia–hypoglycemia, respectively. This retardation in calcium accumulation may be involved in the mechanisms by which propentofylline diminishes ischemic injury.

scholarly journals Resveratrol Promotes Mitochondrial Biogenesis and Protects against Seizure-Induced Neuronal Cell Damage in the Hippocampus Following Status Epilepticus by Activation of the PGC-1α Signaling Pathway

2019 ◽  
Vol 20 (4) ◽  
pp. 998 ◽  
Author(s):  
Yao-Chung Chuang ◽  
Shang-Der Chen ◽  
Chung-Yao Hsu ◽  
Shu-Fang Chen ◽  
Nai-Ching Chen ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Signaling Pathway ◽  
Mitochondrial Biogenesis ◽  
Neuronal Damage ◽  
Cell Damage ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Protective Mechanism ◽  
Protective Effects ◽  
Prolonged Seizure

Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is known to regulate mitochondrial biogenesis. Resveratrol is present in a variety of plants, including the skin of grapes, blueberries, raspberries, mulberries, and peanuts. It has been shown to offer protective effects against a number of cardiovascular and neurodegenerative diseases, stroke, and epilepsy. This study examined the neuroprotective effect of resveratrol on mitochondrial biogenesis in the hippocampus following experimental status epilepticus. Kainic acid was microinjected into left hippocampal CA3 in Sprague Dawley rats to induce bilateral prolonged seizure activity. PGC-1α expression and related mitochondrial biogenesis were investigated. Amounts of nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (Tfam), cytochrome c oxidase 1 (COX1), and mitochondrial DNA (mtDNA) were measured to evaluate the extent of mitochondrial biogenesis. Increased PGC-1α and mitochondrial biogenesis machinery after prolonged seizure were found in CA3. Resveratrol increased expression of PGC-1α, NRF1, and Tfam, NRF1 binding activity, COX1 level, and mtDNA amount. In addition, resveratrol reduced activated caspase-3 activity and attenuated neuronal cell damage in the hippocampus following status epilepticus. These results suggest that resveratrol plays a pivotal role in the mitochondrial biogenesis machinery that may provide a protective mechanism counteracting seizure-induced neuronal damage by activation of the PGC-1α signaling pathway.

scholarly journals Xylazine regulates the release of glycine and aspartic acid in rat brain

2018 ◽  
Vol 62 (1) ◽  
pp. 121-128
Author(s):  
Yi-Ming Zhang ◽  
Dong-Xu Yu ◽  
Bai-Shuang Yin ◽  
Xin-Ran Li ◽  
Li-Na Li ◽  
...  
Keyword(s):  
Aspartic Acid ◽  
Brain Area ◽  
Brain Regions ◽  
Inhibitory Effect ◽  
Test Methods ◽  
Control Group ◽  
Clinical Anaesthesia ◽  
Induced Changes ◽  
Dose Dependent

AbstractIntroductionXylazine, a type of α2-adrenoceptors, is a commonly used drug in veterinary medicine. Xylazine-induced changes in the content of amino acid neurotransmitters – glycine (Gly) and aspartic acid (Asp), in different brain regions and neurons were studied.Material and MethodsWistar rats were administered 50 mg/kg or 70 mg/kg of xylazine by intraperitoneal injection. In addition, in vitro experiments were conducted, in which neurons were treated with 15 μg/mL, 25 μg/mL, 35μg/mL, and 45 μg/mL of xylazine. Test methods were based on the enzyme-linked immunosorbent assays (ELISA).ResultsDuring anaesthesia, Asp levels in each brain area were significantly lower compared to the control group. Except for the cerebrum, levels of Gly in other brain areas were significantly increased during the anaesthesia period. In vitro, xylazine-related neuron secretion of Gly increased significantly compared to the control group at 60 min and 90 min. Moreover, xylazine caused a significant decrease in the levels of Asp secreted by neurons at 20 min, but gradually returned to the level of the control group.ConclusionThe data showed that during anaesthesia the overall levels of Asp decreased and overall levels of Gly increased. In addition, the inhibitory effect of xylazine on Asp and the promotion of Gly were dose-dependent. Our data showed that different effects of xylazine on excitatory and inhibitory neurotransmitters provided a theoretical basis for the mechanism of xylazine activity in clinical anaesthesia.

scholarly journals In VivoAntioxidant Activity of Deacetylasperulosidic Acid in Noni

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
De-Lu Ma ◽  
Mai Chen ◽  
Chen X. Su ◽  
Brett J. West
Keyword(s):  
Antioxidant Activity ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Catalase Activity ◽  
Antioxidant Properties ◽  
Superoxide Dismutase Activity ◽  
Morinda Citrifolia ◽  
Control Group ◽  
Dose Dependent

Deacetylasperulosidic acid (DAA) is a major phytochemical constituent ofMorinda citrifolia(noni) fruit. Noni juice has demonstrated antioxidant activityin vivoand in human trials. To evaluate the role of DAA in this antioxidant activity, Wistar rats were fed 0 (control group), 15, 30, or 60 mg/kg body weight per day for 7 days. Afterwards, serum malondialdehyde concentration and superoxide dismutase and glutathione peroxidase activities were measured and compared among groups. A dose-dependent reduction in malondialdehyde was evident as well as a dose-dependent increase in superoxide dismutase activity. DAA ingestion did not influence serum glutathione peroxidase activity. These results suggest that DAA contributes to the antioxidant activity of noni juice by increasing superoxide dismutase activity. The fact that malondialdehyde concentrations declined with increased DAA dose, despite the lack of glutathione peroxidase-inducing activity, suggests that DAA may also increase catalase activity. It has been previously reported that noni juice increases catalase activityin vivobut additional research is required to confirm the effect of DAA on catalase. Even so, the current findings do explain a possible mechanism of action for the antioxidant properties of noni juice that have been observed in human clinical trials.

scholarly journals Potentials of intravenous laser blood irradiation to correct peroxidation and antioxidant activity as a result of surgical distress

2021 ◽  
Vol 25 (2) ◽  
pp. 22-27
Author(s):  
L. V. Musikhin ◽  
V. S. Shiryaev ◽  
F. M. Shvetsky ◽  
V. I. Potievskaya ◽  
M. B. Potievsky ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Antioxidant Activity ◽  
Optical Density ◽  
Control Group ◽  
Protective Effects ◽  
Sh Groups ◽  
Endogenous Intoxication ◽  
Group I ◽  
Blood Irradiation ◽  
Laser Blood Irradiation

Purpose: to reveal protective effects of intravenous low-level laser blood irradiation (ILBI) during surgical interventions at the gallbladder as well as to study the state of antioxidant activity, lipid peroxidation and endogenous intoxication.Material and methods. In the perioperative period, 40 patients from the main group (I) had traditional treatment which included pharmacological preparations and sessions of intravenous laser blood irradiation. 45 patients from the control group (II) had only traditional (pharmacotherapeutic) treatment. In both groups during surgery, the anesthetic protection consisted of classical neuroleptanalgesia. The age of patients in both groups did not differ significantly. Intravenous laser blood irradiation was done with helium-neon laser “Atoll” 632 nm (Fokon Ltd, St-Petersburg, Russia). During surgery, three irradiation sessions were performed at radiation power of 20 mW and exposure 15 minutes at various stages of surgery: 30 minutes before induction of anesthesia, at the traumatic stage and 30 minutes before the expected finish of the surgery. Ceruloplasmin and transferrin levels in the blood plasma were assessed with the electron paramagnetic resonance technique. The ratio of ceruloplasmin/transferrin which characterizes the level of antioxidant activity was also established. The level of endogenous intoxication was assessed using the previously published technique. The quantitative characteristics of endogenous intoxication by this technique is the value of optical density (D280) and total optical density of components related to high molecular weight and low molecular weight fractions.Results. ILBI sessions in patients neutralize changes in the level of ceruloplasmin and transferrin in blood. The data obtained also confirm ILBI protective effects at protein SH-groups or activation of the restoration of protein SH-groups that were damaged by oxidation as a result of surgical aggression and trauma.Conclusion. The protective effect of intravenous laser blood irradiation in addition to the standard preoperative therapy optimizes pharmacological anesthetic protection during surgery under the existing traditional schemes of combined general anesthesia.

Research on the Correlation between Neuronal Damage and Drug Resistance Gene Product P-Gp Following Status Epilepsy

2012 ◽  
Vol 550-553 ◽  
pp. 1010-1013
Author(s):  
Song Yan Liu ◽  
Rui Tao Mao ◽  
Hua Cai ◽  
Xue Mei Han
Keyword(s):  
Drug Resistance ◽  
Image Analysis ◽  
Status Epilepticus ◽  
Neuronal Damage ◽  
Intractable Epilepsy ◽  
Neuronal Injury ◽  
Control Group ◽  
Analysis Method ◽  
Image Analysis Method ◽  
P Glycoprotein

Objective: To study the association between neuronal injury following status epilepsy and expression of P-glycoprotein, discuss the association between intractable epilepsy and neuronal injury. Method: To establish a mice status epilepticus model by lithium-pilocarpine injected intraperitoneal, The mice were randomly divided into control group 6h, 12h, 1d, 3d, 5d and 7d after status epilepticus(SE) .To research the neuronal injury by image analysis method, expression of P-gp in blood was studied by flow cyometry .To analyze the association between neuronal injury and expression of P-gp by Pearson statistics. Result: The neuronal injury was observed after status epilepsy. Neuronal injury is most obvious 3-7 days after status epilepsy, expression of P-gp increased simultaneously. The severity of neuronal injury has a positive correlation to expression of P-gp. Conclusion: Association between intractable epilepsy and neuronal injury exists.

scholarly journals Cellular and Molecular Evidence of Acetaldehyde Elimination and Intracellular Environment Antioxidation by L-Cysteine

2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Zhenjing Li ◽  
Xiaohong Zhang ◽  
Yibin Xue ◽  
Jingkai Zhang ◽  
Meiling Li ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
A549 Cells ◽  
Control Group ◽  
Molecular Evidence ◽  
Protective Mechanism ◽  
Colorimetric Determination ◽  
Dependent Manner ◽  
Protective Effects ◽  
Dapi Staining ◽  
Dose Dependent

Acetaldehyde is a harmful metabolite of smoking and drinking. This study was initially intended to facilitate the understanding of the possible injury mechanism of A549 cells damaged by acetaldehyde and the possible protective mechanism of L-cysteine (L-Cys) by analyzing the oxidative damage indicators, as well as the changes in cell morphology and gene expression. Results from the dithiodimorpholine nitrobenzoic acid colorimetric determination for glutathione peroxidase (GSH-Px) activity in L-Cys groups were significantly higher (P<0.01) than those in the acetaldehyde group in a dose-dependent manner. The expression of cytochrome c oxidase subunit II (COII) mRNA was significantly reduced compared with the control group (P<0.01) and was noticeably restored in the L-Cys groups. Scanning electronic microscopy observation, DAPI staining, and flow cytometry also indicated that L-Cys could effectively attenuate the oxidative damage to A549 cells caused by acetaldehyde and reduces the rate of apoptosis. In conclusion, the protective effects of L-Cys on A549 cells against oxidative damage by acetaldehyde were dose-dependent within the range of 10 μmol/L to 160 μmol/L. Acetaldehyde damaged the mitochondria and resulted in the apoptosis of A549 cells by reactive oxygen species (ROS), e.g., free radicals, but L-Cys reversed the release of cytochrome c from the mitochondria, reduced the rate of apoptosis, and protected cells from ROS and oxidative stress.

Hepatoprotective and antioxidant activity of hydromethanolic extract of Daniella oliveri leaves in carbon tetrachloride-induced hepatotoxicity in rats

2015 ◽  
Vol 26 (5) ◽  
Author(s):  
Samuel Okwudili Onoja ◽  
Gideon Kelechi Madubuike ◽  
Maxwell Ikechukwu Ezeja
Keyword(s):  
Antioxidant Activity ◽  
Carbon Tetrachloride ◽  
Negative Control Group ◽  
Hepatoprotective Activity ◽  
Negative Control ◽  
Control Group ◽  
Photometric Assay ◽  
Dose Dependent Increase ◽  
Dose Dependent

AbstractThe hepatoprotective activity was investigated using carbon tetrachloride (CClThe pretreatment with extract (100, 200, and 400 mg/kg) and silymarin (100 mg/kg) produced a significant (p<0.05) dose-dependent increase in hepatoprotective activity when compared with the negative control group. The extract (25–400 μg/mL concentration) produced a concentration-dependent increase in antioxidant activity in 2, 2-diphenyl-1-picrylhydrazine (DPPH) photometric assay. The ICThe results of the study suggest that

Protective effects of C-phycocyanin against kainic acid-induced neuronal damage in rat hippocampus

1999 ◽  
Vol 276 (2) ◽  
pp. 75-78 ◽  
Author(s):  
Victor Rimbau ◽  
Antoni Camins ◽  
Cheyla Romay ◽  
Ricardo González ◽  
Mercè Pallàs
Keyword(s):  
Kainic Acid ◽  
Neuronal Damage ◽  
Rat Hippocampus ◽  
Protective Effects

scholarly journals Assessment of mutagenic and antimutagenic effects of Punica granatum in mice

2010 ◽  
Vol 46 (1) ◽  
pp. 121-127 ◽  
Author(s):  
Marize Campos Valadares ◽  
Enir Raquel Tavares Pereira ◽  
Polyana Lopes Benfica ◽  
José Realino Paula
Keyword(s):  
Oxidative Dna Damage ◽  
Punica Granatum ◽  
Control Group ◽  
Dependent Manner ◽  
Protective Effects ◽  
Genotoxic Effects ◽  
Fruit Extract ◽  
Mutagenic Effects ◽  
Dose Dependent ◽  
Ethanolic Leaf Extract

In the present study, the ability of Punica granatum ethanolic leaf extract (PGL) and Punica granatum ethanolic fruit extract (PGF) to induce mutagenicity or to modulate the genotoxic effects induced by the alkylating agent cyclophosphamide (CP) was evaluated. Swiss male mice were treated by gavage for 10 days with PGL or PGF (12.5, 25, 50, and 75 mg/kg/day) prior to exposure to CP (i.p. 200 mg/kg), 24 h after the end of the treatment. Initial observations revealed that normal mice treated with both extracts (12.5, 25, 50, and 75 mg/kg/day) showed a similar micronucleated polychromatic erythrocyte (MNPCE) frequency to that of the control group. Investigation of the protective effect of PGL and PGF based on data analysis revealed that, irrespective of dose or extract, oral administration of PGL or PGF for 10 days prior to exposure had reduced, in a dose-dependent manner, the frequency of MNPCE induced by CP in all groups studied. Higher reductions were observed at PGF doses of 50 and 75 mg/kg. Taken together, these results demonstrate that mice treated with P. granatum showed an absence of mutagenic effects and dose-dependent protective effects against CP-induced oxidative DNA damage.

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