Neuroprotective effect of quercetin in ectoenzymes and acetylcholinesterase activities in cerebral cortex synaptosomes of cadmium-exposed rats

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.

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Neuroprotective Effect of Melatonin Against PCBs Induced Behavioural, Molecular and Histological Changes in Cerebral Cortex of Adult Male Wistar Rats

Neurochemical Research ◽

10.1007/s11064-016-2087-6 ◽

2016 ◽

Vol 42 (2) ◽

pp. 428-438 ◽

Cited By ~ 8

Author(s):

S. Bavithra ◽

K. Selvakumar ◽

L. Sundareswaran ◽

J. Arunakaran

Keyword(s):

Cerebral Cortex ◽

Adult Male ◽

Wistar Rats ◽

Neuroprotective Effect ◽

Histological Changes ◽

Male Wistar Rats

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Attenuation of cerebral vasospasm and secondary injury by 17β-estradiol following experimental subarachnoid hemorrhage

Journal of Neurosurgery ◽

10.3171/2008.6.17622 ◽

2009 ◽

Vol 110 (3) ◽

pp. 457-461 ◽

Cited By ~ 5

Author(s):

Chih-Lung Lin ◽

Aaron S. Dumont ◽

Yu-Feng Su ◽

Yee-Jean Tsai ◽

Jih-Hui Huang ◽

...

Keyword(s):

Cerebral Cortex ◽

Subarachnoid Hemorrhage ◽

Dentate Gyrus ◽

Dna Fragmentation ◽

Cerebral Vasospasm ◽

Neuroprotective Effect ◽

Major Complication ◽

Secondary Injury ◽

Cross Sectional ◽

17Β Estradiol

Object Cerebral vasospasm remains a major complication in patients who have suffered a subarachnoid hemorrhage (SAH). Previous studies have shown that 17β-estradiol (E2) attenuates experimental SAH–induced cerebral vasospasm. Moreover, E2 has been shown to reduce neuronal apoptosis and secondary injury following cerebral ischemia. Adenosine A1 receptor (AR-A1) expression is increased following ischemia and may represent an endogenous neuroprotective effect. This study was designed to evaluate the efficacy of E2 in preventing cerebral vasospasm and reducing secondary injury, as evidenced by DNA fragmentation and AR-A1 expression, following SAH. Methods A double-hemorrhage model of SAH in rats was used, and the degree of vasospasm was determined by averaging the cross-sectional areas of the basilar artery 7 days after the first SAH. A cell death assay was used to detect apoptosis. Changes in the protein expression of AR-A1 in the cerebral cortex, hippocampus, and dentate gyrus were compared with levels in normal controls and E2-treated groups (subcutaneous E2, 0.3 mg/ml). Results The administration of E2 prevented vasospasm (p < 0.05). Seven days after the first SAH, DNA fragmentation and protein levels of AR-A1 were significantly increased in the dentate gyrus. The E2 treatment decreased DNA fragmentation and prevented the increase in AR-A1 expression in the dentate gyrus. There were no significant changes in DNA fragmentation and the expression of AR-A1 after SAH in the cerebral cortex and hippocampus in the animals in the control and E2-treated groups. Conclusions The E2 was effective in attenuating SAH-induced cerebral vasospasm, decreasing apoptosis in the dentate gyrus, and reducing the expression of AR-A1 in the dentate gyrus after SAH. Interestingly, E2 appears to effectively prevent cerebral vasospasm subsequent to SAH as well as attenuate secondary injury by reducing both apoptosis and a compensatory increase in AR-A1 expression in the dentate gyrus.

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NEUROPROTECTIVE EFFECTS OF POMEGRANATE JUICE ON LEAD INDUCED NEUROTOXICITY IN MICE

International Journal of Pharmacy and Pharmaceutical Sciences ◽

10.22159/ijpps.2017v9i2.15806 ◽

2017 ◽

Vol 9 (2) ◽

pp. 207

Author(s):

Leila Gadouche ◽

Noureddine Djebli ◽

Khayra Zerrouki

Keyword(s):

Drinking Water ◽

Cerebral Cortex ◽

Lead Acetate ◽

Neuronal Degeneration ◽

Neuroprotective Effect ◽

Pomegranate Juice ◽

Total Phenolic ◽

Control Group ◽

Histological Structure ◽

Neuroprotective Effects

Objective: This study evaluates the potential neuroprotective of the pomegranate juice against chronic intoxication with lead acetate for 3 months.Methods: Twenty-one female Swiss mice divided into 3 groups were employed in the present investigation. Control group: received drinking water for 90 days, neurotoxic group were exposed to 1000 ppm of lead acetate in the drinking water for 12 weeks, and neurotoxic treated group represents the mice received treatment with juice pomegranate diluted with distilled water (v/v) orally for 4 h / day followed by lead acetate at a dose of 1000 ppm orally for 20 h / day for 90 days. After cessation of treatment, neurobehavioral studies using the open field test, black and white test box and swimming test were made. In the next phase, brain injury was assessed histologically with hematoxylin-eosin staining.Results: Chronic exposure to lead led to significant increase in the level of anxiety, depression and the locomotor activity (P < 0.05). It was confirmed by histopathological alterations in many areas of the cerebral cortex and hippocampus including neuronal degeneration and decrease cell density. Treatment with the juice significantly improve the level of depression, locomotor function (P < 005) and anxiety (P > 0.05) in mice exposed to lead as well as restored the histological structure in cerebral cortex and hippocampus of mice. The total phenolic and flavonoids content in juice of pomegranate was found to be 3809. 8±29.404 mg GAE/l; 2109. 57±18.936 mg QE /l of juice.Conclusion: This finding suggests that phenolic compounds found in pomegranate juice provide a neuroprotective effect on behavioural impairments and histopathological change induced by lead.

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Neuroprotective effect of Gracilaria corticata against aluminium-induced neurotoxicity in the hippocampus and cerebral cortex of rat brain: Biochemical and histological approach

Asian Journal of Pharmacy and Pharmacology ◽

10.31024/ajpp.2019.5.3.24 ◽

2019 ◽

Vol 5 (3) ◽

pp. 604-613

Author(s):

Asha Chacko ◽

Sibi P. Ittiyavirah

Keyword(s):

Cerebral Cortex ◽

Rat Brain ◽

Neuroprotective Effect ◽

Gracilaria Corticata

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Neuroprotective Effect of Physical Exercise on Neuronal Apoptosis Induced by Tramadol in Cerebral Cortex of Rats

Biointerface Research in Applied Chemistry ◽

10.33263/briac106.72097222 ◽

2020 ◽

Vol 10 (6) ◽

pp. 7209-7222

Keyword(s):

Oxidative Stress ◽

Cerebral Cortex ◽

Physical Exercise ◽

Cortical Neurons ◽

Neuronal Apoptosis ◽

Neuroprotective Effect ◽

Physiological Saline ◽

Male Rats ◽

Control Group ◽

Oxidative Stress Biomarkers

Tramadol is a centrally acting analgesic agent with low affinity for opioid receptors, used for treating moderate to severe pain. Tramadol, like other opioids, induces neuronal apoptosis, which causes multiple neuronal impairments. The current study was conducted to evaluate the potential neuroprotective role of physical exercises on tramadol-induced neuronal apoptosis in the cerebral cortex of rats. Thirty adult male rats were divided into three groups (n= 10) as follow; the control group was gavaged with physiological saline (0.9% NaCl); tramadol group was daily administered with tramadol (40 mg/kg) for 28 days, and physical exercise group was administered with the same dose as tramadol group, then rats were forced to run on the treadmill for 30 min, once a day for 28 days. Tramadol induced histopathological changes in the form of neuroses degeneration and apoptosis. These findings were confirmed by immunohistochemical and blotting studies, which showed upregulation of p53 and downregulation of Bcl-2. In addition, malondialdehyde (MDA), myeloperoxidase (MPO), and nuclear factor kappa B (NF-κB) significantly increased following tramadol administration. At the same time, glutathione (GSH) and glutathione peroxidase (GPx) were decreased. In contrast, physical exercise was found to protect cortical neurons from degeneration and apoptosis produced by tramadol. This was evidenced by the downregulation of p53 and upregulating Bcl-2 expression and the improved changes in the oxidative stress biomarkers in rats. Physical exercise reduced the neuronal apoptosis and degeneration in the cerebral cortex following tramadol administration through suppressing oxidative stress.

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Tumor necrosis factor-alpha - potential target for neuroprotector dimebon

Biomeditsinskaya Khimiya ◽

10.18097/pbmc20166204418 ◽

2016 ◽

Vol 62 (4) ◽

pp. 418-425 ◽

Cited By ~ 1

Author(s):

A.V. Alessenko ◽

S.O. Bachurin ◽

S.V. Gurianova ◽

Y.O. Karatasso ◽

E.F. Shevtsova ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cerebral Cortex ◽

Molecular Species ◽

Animal Studies ◽

Neuroprotective Effect ◽

New Drugs ◽

Necrosis Factor Alpha ◽

Positive Effects ◽

New Therapeutic Approaches

Dimebon (Dimebolin) is an antihistamine drug which has been used in Russia since 1983. Recently Dimebolin has attracted renewed interest after being shown to have positive effects on persons suffering from Alzheimer's disease. Animal studies have shown that dimebon acts through multiple mechanisms, both blocking the action of neurotoxic beta-amyloid peptides and inhibiting L-type calcium channels, modulating the action of AMPA and NMDA glutamate receptors. Our experiments with cell culture L929 and mice have shown that dimebon may exert its neuroprotective effect by blocking cytotoxic signals induced by proinflammatory cytokines such as TNF-a which are believed to play a central role in Alzheimer's disease. Dimebon (10 mg/ml) protected mouse fibroblasts L929 against the toxic action of TNF-a. Our study included 65 male mice. TNF-a (10 mg per mouse), dimebon (0,2 mg/kg) and their combination were injected intraperitonealy. Changes in the level of molecular species of sphingomyelin and galactosyl ceramide in hippocampus, cerebellum and cerebral cortex within 30 min, 2 h, 4 h, and 24 h after injection were detected by chromato-mass-spectrometry. Maximal changes in sphingomyelin and galactosyl ceramides contents of different molecular species after single TNF-a administration were found in the hippocampus, and were less expressed in the cerebral cortex and cerebellum after 24 h. Dimebon itself did not induce changes in the sphingolipid spectrum in brain sections, but protected them against disorders induced by TNF-a in the brain. Modern strategies in the search of new therapeutic approaches are based on the multitarget properties of new drugs. According to our results TNF-a may serve as a new target for dimebon.

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Neuroprotective effect of resveratrol on arsenic trioxide–induced oxidative stress in feline brain

Human & Experimental Toxicology ◽

10.1177/0960327113506235 ◽

2013 ◽

Vol 33 (7) ◽

pp. 737-747 ◽

Cited By ~ 8

Author(s):

Y Cheng ◽

J Xue ◽

H Jiang ◽

M Wang ◽

L Gao ◽

...

Keyword(s):

Cerebral Cortex ◽

Oxidative Damage ◽

Arsenic Trioxide ◽

Reduced Glutathione ◽

Neuroprotective Effect ◽

Arsenic Exposure ◽

Physiological Saline ◽

Treated Group ◽

Contaminated Water ◽

Clinical Use

Arsenic trioxide (As2O3) is a known environmental toxicant and potent chemotherapeutic agent. Significant correlation has been reported between arsenic exposure (including consumption of arsenic-contaminated water and clinical use of As2O3) and dysfunction in the nervous system. In this study, we aimed to elucidate the effect of resveratrol with neuroprotective activities on As2O3-induced oxidative damage and cerebral cortex injury. Twenty-four healthy Chinese Dragon Li cats of either sex were randomly divided into four groups: control (1 ml/kg physiological saline), As2O3 (1 mg/kg), resveratrol (3 mg/kg) and As2O3 (1 mg/kg) + resveratrol (3 mg/kg). As2O3+resveratrol-treated group were given resveratrol (3 mg/kg) 1 h before As2O3 (1 mg/kg) administration. Pretreatment with resveratrol upregulated the activities of antioxidant enzymes and attenuated As2O3-induced increases in reactive oxygen species and malondialdehyde production. In addition, resveratrol attenuated the As2O3-induced reduction in the level of reduced glutathione and the ratio of reduced glutathione to oxidised glutathione, and accumulation of arsenic in the cerebral cortex. These findings support neuroprotective effect of resveratrol on As2O3 toxicity in feline brain and provide a better understanding of the mechanism that resveratrol modulates As2O3-induced oxidative damage and a stronger rational for clinical use of resveratrol to protect brain against the toxicity of arsenic.

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