scholarly journals In Vitro Antioxidant Activity of Purple Grape Juice (Vitis Labrusca) against Temozolamide Treatment in Rat Brains

Beverages ◽  
2018 ◽  
Vol 4 (4) ◽  
pp. 99
Author(s):  
Tatiane Gabardo ◽  
Marina Rocha Frusciante ◽  
Jessica Pereira Marinho ◽  
Manuela dos Santos ◽  
Ana Abujamra ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Protein Oxidation ◽  
Neuroprotective Effect ◽  
Grape Juice ◽  
Thiobarbituric Acid ◽  
Redox Balance ◽  
Sod Activity ◽  
The Central Nervous System ◽  
In Vitro Antioxidant Activity

Considering that grape juice has high levels of phenolic compounds that produce beneficial physiological effects, important for the maintenance of redox balance, the aim of this study was to evaluate the in vitro neuroprotective effect of purple grape juice on the oxidative damage caused by temozolomide (TMZ) in the cerebral cortex, hippocampus, and cerebellum of Wistar rats. In pre-incubation, TMZ increased thiobarbituric acid reactive substances (TBARS) in the cerebral cortex and cerebellum, enhanced protein oxidation in all tissues studied, increased superoxide dismutase (SOD) activity in the hippocampus, decreased SOD activity in the cerebellum, and enhanced catalase (CAT) activity in the cerebral cortex and cerebellum. In co-incubation, there was enhanced protein oxidation in the cerebral cortex and cerebellum, decreased SOD activity in the cerebellum, inhibition of CAT activity in the hippocampus, and increased CAT activity in the cerebellum. Purple grape juice improved these oxidative alterations. Therefore, the intake of grape juice might have a protective effect against diseases that affect the oxidative status of the central nervous system.

scholarly journals Exploring the Use of Dimethyl Fumarate as Microglia Modulator for Neurodegenerative Diseases Treatment

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 700
Author(s):  
Maria Rosito ◽  
Claudia Testi ◽  
Giacomo Parisi ◽  
Barbara Cortese ◽  
Paola Baiocco ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Iron Homeostasis ◽  
Brain Injuries ◽  
Neuroprotective Effect ◽  
Redox Homeostasis ◽  
Dimethyl Fumarate ◽  
Redox Balance ◽  
Fumaric Acid Ester ◽  
The Central Nervous System

The maintenance of redox homeostasis in the brain is critical for the prevention of the development of neurodegenerative diseases. Drugs acting on brain redox balance can be promising for the treatment of neurodegeneration. For more than four decades, dimethyl fumarate (DMF) and other derivatives of fumaric acid ester compounds have been shown to mitigate a number of pathological mechanisms associated with psoriasis and relapsing forms of multiple sclerosis (MS). Recently, DMF has been shown to exert a neuroprotective effect on the central nervous system (CNS), possibly through the modulation of microglia detrimental actions, observed also in multiple brain injuries. In addition to the hypothesis that DMF is linked to the activation of NRF2 and NF-kB transcription factors, the neuroprotective action of DMF may be mediated by the activation of the glutathione (GSH) antioxidant pathway and the regulation of brain iron homeostasis. This review will focus on the role of DMF as an antioxidant modulator in microglia processes and on its mechanisms of action in the modulation of different pathways to attenuate neurodegenerative disease progression.

scholarly journals Neuroprotective Effect of Radix Trichosanthis Saponins on Subarachnoid Hemorrhage

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Ying Chen ◽  
Haiyan Sun ◽  
Liyong Huang ◽  
Juxiang Li ◽  
Wenke Zhou ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Subarachnoid Hemorrhage ◽  
Neuroprotective Effect ◽  
Free Radical Scavengers ◽  
Therapeutic Modality ◽  
Sod Activity ◽  
Neuroprotective Effects ◽  
P53 Expression

Redox homeostasis has been implicated in subarachnoid hemorrhage (SAH). As a result, antioxidants and/or free radical scavengers have become an important therapeutic modality. Considering that radix trichosanthis (RT) saponins exhibited strong antioxidant ability bothin vivoandin vitro, the present study aimed to reveal whether the neuroprotective activities of RT saponins were mediated by p38/p53 signal pathway after SAH. An established SAH model was used and superoxide dismutase (SOD), malondialdehyde (MDA), induced nitric oxide synthase (iNOS), nitric oxide (NO), lactate dehydrogenase (LDH), p-p38, and p53 activation were detected after 48 h of SAH. The results showed that RT saponins inhibited iNOS expression to restore NO to basal level. Moreover, compared with Cu/Zn-SOD, RT saponins (2 mg/kg/d dosage) significantly increased Mn-SOD activity after SAH. Accompanied with lowered NO and elevated SOD, decreased p38 phosphorylation and p53 activities were observed, especially for RT saponins at 2 mg/kg/d dosage. In this setting, the neurological outcome was also improved with less neuronal cells damage after RT saponins pretreatment. Our findings demonstrated the beneficial effects of RT saponins in enhancing neuroprotective effects by deducing iNOS activity, normalizing SOD level, and inhibiting p-p38 and p53 expression, hence offering significant therapeutic implications for SAH.

The Neuroprotective Effect of Picroside II from Hu-Huang-Lian against Oxidative Stress

2007 ◽  
Vol 35 (04) ◽  
pp. 681-691 ◽  
Author(s):  
Ting Li ◽  
Jian-Wen Liu ◽  
Xiao-Dong Zhang ◽  
Ming-Chuan Guo ◽  
Guang Ji
Keyword(s):  
Oxidative Stress ◽  
Pc12 Cells ◽  
Therapeutic Potential ◽  
Neuroprotective Effect ◽  
Active Constituent ◽  
Sod Activity ◽  
Picroside Ii ◽  
Pre Treatment

Picroside II is an active constituent extracted from the traditional Chinese medicine (TCM) Hu-Huang-Lian. To evaluate the neuroprotective effect of picroside II, PC12 cells were treated with glutamate in vitro and male ICR mice were treated with AlCl 3in vivo. Pre-treatment of PC12 cells with picroside II could enhance the cell viability and decrease the level of intracellular reactive oxygen species (ROS) induced by glutamate. By DNA fragmentation and flow cytometry assay, picroside II (1.2 mg/ml) significantly prevented glutamate-induced cell apoptosis. In the animal study, amnesia was induced in mice by AlCl 3 (100 mg/kg/d, i.v.). Pricroside II, at the dose of 20 and 40 mg/kg/d (i.g.), markedly ameliorated AlCl 3-induced learning and memory dysfunctions and attenuated AlCl 3-induced histological changes. This was associated with the significant increased superoxide dismutase (SOD) activity in the brain of experimental mice. All these results indicated that picroside II possessed the therapeutic potential in protecting against neurological injuries damaged by oxidative stress.

scholarly journals Salsolinol—neurotoxic or Neuroprotective?

2019 ◽  
Vol 37 (2) ◽  
pp. 286-297 ◽  
Author(s):  
Magdalena Kurnik-Łucka ◽  
Gniewomir Latacz ◽  
Adrian Martyniak ◽  
Andrzej Bugajski ◽  
Katarzyna Kieć-Kononowicz ◽  
...  
Keyword(s):  
Dopaminergic Neurons ◽  
Neuroprotective Effect ◽  
Serum Levels ◽  
In Vivo Experiments ◽  
Pathophysiological Role ◽  
The Central Nervous System ◽  
Significant Release ◽  
6 Hydroxydopamine

AbstractSalsolinol (6,7-dihydroxy-1-methyl-1,2,3,4-tetrahydroisoquinoline), widely available in many edibles, is considered to alter the function of dopaminergic neurons in the central nervous system and thus, multiple hypotheses on its either physiological and/or pathophysiological role have emerged. The aim of our work was to revisit its potentially neurotoxic and/or neuroprotective role through a series of both in vitro and in vivo experiments. Salsolinol in the concentration range 10–250 μM did not show any significant release of lactate dehydrogenase from necrotic SH-SY5Y cells and was able in the concentration of 50 and 100 μM to rescue SH-SY5Y cells from death induced by H2O2. Its neuroprotective effect against neurotoxin 6-hydroxydopamine was also determined. Salsolinol was found to decrease significantly the reactive oxygen species level in SH-SY5Y cells treated by 500 μM H2O2 and the caspase activity induced by 300 μM of H2O2 or 100 μM of 6-hydroxydopamine. Serum levels of TNFα and CRP of salsolinol-treated rats were not significantly different from control animals. Both TNFα and CRP served as indirect markers of neurotoxicity and/or neuroprotection. Although the neurotoxic properties of salsolinol have numerously been emphasized, its neuroprotective properties should not be neglected and need greater consideration.

scholarly journals Brain peptides and glial growth. I. Glia-promoting factors as regulators of gliogenesis in the developing and injured central nervous system.

1986 ◽  
Vol 102 (3) ◽  
pp. 803-811 ◽  
Author(s):  
D Giulian ◽  
R L Allen ◽  
T J Baker ◽  
Y Tomozawa
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Cell Growth ◽  
Stab Wound ◽  
Mammalian Brain ◽  
Brain Peptides ◽  
Regulate Cell Growth ◽  
The Central Nervous System

Glia-promoting factors (GPFs) are peptides of the central nervous system which accelerate the growth of specific glial populations in vitro. Although these factors were first discovered in the goldfish visual system (Giulian, D., Y. Tomozawa, H. Hindman, and R. Allen, 1985, Proc. Natl. Acad. Sci. USA., 83:4287-4290), we now report similar peptides are found in mammalian brain. The cerebral cortex of rat contains oligodendroglia-stimulating peptides, GPF1 (15 kD) and GPF3 (6 kD), as well as astroglia-stimulating peptides, GPF2 (9 kD) and GPF4 (3 kD). The concentrations of specific GPFs increase in brain during periods of gliogenesis. For example, GPF1 and GPF3 are found in postnatal rat brain during a peak of oligondendroglial growth while GPF2 and GPF4 are first detected at a time of astroglial proliferation in the embryo. Stab wound injury to the cerebral cortices of rats stimulates astroglial proliferation and induces marked elevations in levels of GPF2 and GPF4. Our findings suggest that two distinct classes of GPFs, those acting upon oligodendroglia and those acting upon astroglia, help to regulate cell growth in the developing and injured central nervous system.

scholarly journals Increased Oxidative Stress and Imbalance in Antioxidant Enzymes in the Brains of Alloxan-Induced Diabetic Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Luciane B. Ceretta ◽  
Gislaine Z. Réus ◽  
Helena M. Abelaira ◽  
Karine F. Ribeiro ◽  
Giovanni Zappellini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Animal Model ◽  
Antioxidant Enzymes ◽  
Prefrontal Cortex ◽  
Recognition Memory ◽  
Recognition Task ◽  
Thiobarbituric Acid ◽  
Diabetic Rats ◽  
Sod Activity ◽  
The Central Nervous System

Diabetes Mellitus (DM) is associated with pathological changes in the central nervous system (SNC) as well as alterations in oxidative stress. Thus, the main objective of this study was to evaluate the effects of the animal model of diabetes induced by alloxan on memory and oxidative stress. Diabetes was induced in Wistar rats by using a single injection of alloxan (150 mg/kg), and fifteen days after induction, the rats memory was evaluated through the use of the object recognition task. The oxidative stress parameters and the activity of antioxidant enzymes, superoxide dismutase (SOD), and catalase (CAT) were measured in the rat brain. The results showed that diabetic rats did not have alterations in their recognition memory. However, the results did show that diabetic rats had increases in the levels of superoxide in the prefrontal cortex, and in thiobarbituric acid reactive species (TBARS) production in the prefrontal cortex and in the amygdala in submitochondrial particles. Also, there was an increase in protein oxidation in the hippocampus and striatum, and in TBARS oxidation in the striatum and amygdala. The SOD activity was decreased in diabetic rats in the striatum and amygdala. However, the CAT activity was increased in the hippocampus taken from diabetic rats. In conclusion, our findings illustrate that the animal model of diabetes induced by alloxan did not cause alterations in the animals’ recognition memory, but it produced oxidants and an imbalance between SOD and CAT activities, which could contribute to the pathophysiology of diabetes.

scholarly journals Counteracting effects on free radicals and histological alterations induced by a fraction with casearins

2015 ◽  
Vol 87 (3) ◽  
pp. 1791-1807 ◽  
Author(s):  
ÉVERTON JOSÉ FERREIRA DE ARAÚJO ◽  
GUILHERME ANTÔNIO LOPES DE OLIVEIRA ◽  
LÍVIA QUEIROZ DE SOUSA ◽  
VANDERLAN DA SILVA BOLZANI ◽  
ALBERTO JOSÉ CAVALHEIRO ◽  
...  
Keyword(s):  
Antioxidant Activities ◽  
Antitumor Activities ◽  
Histological Changes ◽  
Histological Alterations ◽  
Clerodane Diterpenes ◽  
The Central Nervous System ◽  
Casearia Sylvestris ◽  
Tbars Formation ◽  
In Vitro Antioxidant Activity

ABSTRACTCasearia sylvestris Swartz is a medicinal plant widely distributed in Brazil. It has anti-inflammatory, antiulcer and antitumor activities and is popularly used to treat snakebites, wounds, diarrhea, flu and chest colds. Its leaves are rich in oxygenated tricyclic cis-clerodane diterpenes, particulary casearins. Herein, we evaluated the antioxidant activities of a fraction with casearins (FC) isolated from C. sylvestrisand histological changes on the central nervous system and livers of Mus musculus mice. Firstly, in vitro studies (0.9, 1.8, 3.6, 5.4 and 7.2 μg/mL) revealed EC50 values of 3.7, 6.4 and 0.16 µg/mL for nitrite, hydroxyl radical and TBARS levels, respectively. Secondly, FC (2.5, 5, 10 and 25 mg/kg/day) was intraperitoneally administered to Swiss mice for 7 consecutive days. Nitrite levels in the hippocampus (26.2, 27.3, 30.2 and 26.6 µM) and striatum (26.3, 25.4, 34.3 and 27.5 µM) increased in all treated animals (P < 0.05). Lower doses dropped reduced glutathione, catalase and TBARS levels in the hippocampus and striatum. With the exception of this reduction in TBARS formation, FC displayed only in vitro antioxidant activity. Animals exhibited histological alterations suggestive of neurotoxicity and hepatotoxicity, indicating the need for precaution regarding the consumption of medicinal formulations based on Casearia sylvestris.

Effects of intermittent hypoxia different regimes on mitochondrial lipid peroxidation and glutathione-redox balance in stressed rats

2008 ◽  
Vol 3 (3) ◽  
pp. 233-242 ◽  
Author(s):  
Olga Gonchar
Keyword(s):  
Lipid Peroxidation ◽  
Intermittent Hypoxia ◽  
Antioxidant Defense System ◽  
Redox Balance ◽  
Liver Mitochondria ◽  
Sod Activity ◽  
Beneficial Effects ◽  
Late Preconditioning ◽  
Mitochondrial Superoxide

AbstractThe purpose of this study was to compare the influence of two regimes of intermittent hypoxia (IH) [repetitive 5 cycles of 5 min hypoxia (7% O2 or 12% O2 in N2) followed by 15 min normoxia, daily for three weeks] on oxidative stress protective systems in liver mitochondria. To estimate the effectiveness of hypoxia adaptation at the early and late preconditioning period, we exposed rats to acute 6-h immobilization at the 1st and 45th days after cessation of IH. We showed that severity of hypoxic episodes during IH might initiate different adaptive programs. Moderate hypoxia during IH prevents mitochondrial glutathione pool depletion induced by immobilization stress, maintains GSH-redox cycle via activation of glutathione peroxidase, glutathione-S-transferase, glutathione reductase, NADP+-dependent isocitrate dehydrogenase, and increases Mn-SOD activity. Such regimen of hypoxic preconditioning caused the decrease of mitochondrial superoxide anion generation as well as of basal and stimulated in vitro lipid peroxidation and this protective effect remained for 45 days under renormoxic conditions. Hypoxic adaptation in a more severe regimen exerted beneficial effects on the mitochondrial antioxidant defense system only at its later phase.

scholarly journals Oxidative stress biomarkers and acetylcholinesterase activity in human erythrocytes exposed to clomazone (in vitro)

2011 ◽  
Vol 4 (3) ◽  
pp. 149-153 ◽  
Author(s):  
Adriana Santi ◽  
Charlene Menezes ◽  
Marta Duarte ◽  
Jossiele Leitemperger ◽  
Thais Lópes ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Thiobarbituric Acid ◽  
Acetylcholinesterase Activity ◽  
Human Erythrocytes ◽  
Thiobarbituric Acid Reactive Substances ◽  
Oxidative Stress Biomarkers ◽  
Sod Activity ◽  
Stress Biomarkers

Oxidative stress biomarkers and acetylcholinesterase activity in human erythrocytes exposed to clomazone (in vitro)The aim of this study was to investigate the effect of clomazone herbicide on oxidative stress biomarkers and acetylcholinesterase activity in human erythrocytes inin vitroconditions. The activity of catalase (CAT), superoxide dismutase (SOD) and acetylcholinesterase (AChE), as well as the levels of thiobarbituric acid reactive substances (TBARS) and reduced glutathione (GSH) were measured in human erythrocytes exposed (in vitro) to clomazone at varying concentrations in the range of 0, 100, 250 and 500 μg/L for 1 h at 37°C. TBARS levels were significantly higher in erythrocytes incubated with clomazone at 100, 250 and 500 μg/L. However, erythrocyte CAT and AChE activities were decreased at all concentrations tested. SOD activity was increased only at 100 μg/L of clomazone. GSH levels did not change with clomazone exposure. These results clearly showed clomazone to induce oxidative stress and AChE inhibition in human erythrocytes (in vitro). We, thus, suggest a possible role of ROS on toxicity mechanism induced by clomazone in humans.

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