scholarly journals Neuroprotective Effect of Xylopia Aethiopica Seed on Lead-Induced Injury on the Cerebral Cortex of Male Wistar Rat

2021 ◽  
Vol 6 (1) ◽  
pp. 7
Author(s):  
Chinna Nneka Orish ◽  
Samuel Sotonye George ◽  
Eberechi Wogu ◽  
Anthoneth Ndidiamaka Ezejiofor
Keyword(s):  
Cerebral Cortex ◽  
Neuroprotective Effect ◽  
Wistar Rat ◽  
Xylopia Aethiopica

scholarly journals Neuroprotective effect of vitamin E supplementation in wistar rat treated with acrylamide

2012 ◽  
Vol 19 (1) ◽  
pp. 1 ◽  
Author(s):  
Nitin Kurkure ◽  
Vandana Hedaoo ◽  
Santosh Rahangadale ◽  
Baijnath Prajapati ◽  
ArunG Bhandarkar
Keyword(s):  
Vitamin E ◽  
Neuroprotective Effect ◽  
Wistar Rat ◽  
Vitamin E Supplementation

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.

Neuroprotective effect of Lithospermum officinale callus extract on inflamed primary microglial cells

2020 ◽  
Vol 21 ◽  
Author(s):  
Maryam Kheyrollah ◽  
Farzaneh Sabouni ◽  
Mohsen Farhadpour ◽  
Kamahldin Haghbeen
Keyword(s):  
Neuroprotective Effect ◽  
Wistar Rat ◽  
Microglial Cells ◽  
Root Extract ◽  
Primary Microglia ◽  
Methanolic Extracts ◽  
Tnf Α ◽  
The Central Nervous System ◽  
Anti Inflammatory ◽  
Lithospermum Officinale

Background and Objective: Lithospermum officinale is a famous medicinal herb in the traditional medicine of India. However, the medicinal use of its root extract is limited due to the presence of pyrrolizidine alkaloids (PzAl). It was recently shown that PzAl are not accumulated in the cell culture of L. officinale while the biosynthetic pathway of phenolic acids remains active so that rosmarinic acid (RsA) is the main product in the proliferated callus. Considering the existing literature on the anti-inflammatory effects of caffeic acid (CfA) and its derivatives, this research was devoted to the evaluation of the anti-inflammatory capacity of methanolic extracts of L. officinale callus (LoE) on the rat microglial cells as the immune cells of the Central Nervous System, which play an essential role in the responses to neuroinflammation. Methods: primary microglia were obtained from Wistar rat, then they were subjected to various amounts of CfA and methanolic extracts of 17 and 31-day L. officinale callus prior to stimulation by LPS. In addition to HPLC analysis of the extracts, viability, nitric oxide production, evaluation of the pro-inflammatory genes and cytokines in the inflamed microglia were investigated. Results: Methanolic extract of the 17-day old callus of L. officinale exhibited anti-inflammatory effects on the LPS- stimulated microglial cells much higher than that was observed for CfA. The data was further supported by the decreased expression of NOS2, TNF-α, and Cox-2 mRNA and the suppression of TNF-α and IL-1β release in the activated microglial cells pretreated with the effective dose of LoE (0.8 mg mL-1). Conclusion: It was assumed that better anti-neuroinflammatory performance of LoE than CfA in LPS-activated primary microglia could be a result of synergism of the components of the extract and the lipophilic nature of RsA as the main phenolic acid of LoE. Considering the fact that LoE shows high antioxidant capacity and lacks PzAl, it is anticipated that LoE is considered as a reliable substitute to the extract of the natural root of L. officinale and plays a key role in the preparation of neuroprotective pharmaceutical formula.

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

2013 ◽  
Vol 381 (1-2) ◽  
pp. 1-8 ◽  
Author(s):  
Fátima Husein Abdalla ◽  
Andréia Machado Cardoso ◽  
Luciane Belmonte Pereira ◽  
Roberta Schmatz ◽  
Jamile Fabbrin Gonçalves ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Neuroprotective Effect

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

2009 ◽  
Vol 110 (3) ◽  
pp. 457-461 ◽  
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.

scholarly journals NEUROPROTECTIVE EFFECTS OF POMEGRANATE JUICE ON LEAD INDUCED NEUROTOXICITY IN MICE

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

<p><strong>Objective: </strong>This study evaluates the potential neuroprotective of the pomegranate juice against chronic intoxication with lead acetate for 3<strong> </strong>months.</p><p><strong>Methods: </strong>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.</p><p><strong>Results:</strong> Chronic exposure to lead led to significant increase in the level of anxiety, depression and the locomotor activity (P &lt; 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 &lt; 005) and anxiety (P &gt; 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.</p><p><strong>Conclusion: </strong>This finding suggests that phenolic compounds found in pomegranate juice provide a neuroprotective effect on behavioural impairments and histopathological change induced by lead.</p>

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

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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