scholarly journals Oxidative stress in mitochondria of the brain tissue with aluminum neurotoxycosis and applying of glutathione and modulators of coenzyme A biosynthesis

2020 ◽  
Vol 64 (1) ◽  
pp. 78-85
Author(s):  
D. S. Semenovich ◽  
N. P. Kanunnikova ◽  
А. G. Moiseenok
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
Coenzyme A ◽  
The Brain ◽  
Coenzyme A Biosynthesis

scholarly journals High-fat diet-induced obesity and impairment of brain neurotransmitter pool

2020 ◽  
Vol 11 (1) ◽  
pp. 147-160
Author(s):  
Ranyah Shaker M. Labban ◽  
Hanan Alfawaz ◽  
Ahmed T. Almnaizel ◽  
Wail M. Hassan ◽  
Ramesa Shafi Bhat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Obese Group ◽  
Control Group ◽  
High Fat ◽  
Brain Neurotransmitter ◽  
The Brain ◽  
Lean Group

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.

scholarly journals Fangchinoline ameliorates the expressions of angiogenic molecule in cerebral ischemia induced neuronal degeneration in neonatal rats

2018 ◽  
Vol 9 (1) ◽  
pp. 117-122
Author(s):  
Han Daicheng ◽  
Xia Shiwen ◽  
Zhu Huaping ◽  
Liu Yong ◽  
Zhou Qianqian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Cerebral Ischemia ◽  
Brain Tissue ◽  
Neuronal Degeneration ◽  
Neuronal Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Neonatal Rats ◽  
Markers Of Oxidative Stress ◽  
The Brain

AbstractBackgroundPresent investigation evaluates the beneficial effect of fangchinoline on cerebral ischemia induced neuronal degeneration in neonatal rats and also postulates the possible mechanism of its action.MethodologyCerebral ischemia was produced by the ligation of right common carotid artery in neonatal rats on postnatal day 5 (P5) and further pups were treated with fangchinoline 3, 10 and 30 mg/kg, i.p. for the period of 3 days. Effect of fangchinoline was estimated by determining the brain injury and enzyme linked immunosorbent assay (ELISA) method was used for the estimation of pro-inflammatory mediators and markers of oxidative stress in the cerebral tissues of neonatal rats. Moreover western blot assay and histopathology study was also performed on the brain tissue.ResultsResult of this investigation reveals that the percentage of brain injury significantly reduces and enhancement of myelin basic protein in the cerebral tissues of fangchinoline than ischemic group. Treatment with fangchinoline attenuates the altered level of proinflammatory mediators and markers of oxidative stress in the cerebral tissue of cerebral ischemia induced neuronal injury neonatal rats. Moreover expressions of inducible nitric oxide synthtase (iNOS), vascular endothelial growth factor (VEGF), p53 and nuclear receptor factor-2 (Nrf2) in the brain tissue attenuated by fangchinoline treated group.ConclusionIn conclusion, fangchinoline ameliorates the cerebral ischemia induced neuronal injury in neonatal rats by enhancing angiogenesis molecules.

Nigella sativa oil and thymoquinone reduce oxidative stress in the brain tissue of rats exposed to total head irradiation

2019 ◽  
Vol 96 (2) ◽  
pp. 228-235
Author(s):  
Elif Demir ◽  
Seyithan Taysi ◽  
Hasan Ulusal ◽  
Davut Sinan Kaplan ◽  
Kadir Cinar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
Nigella Sativa ◽  
Nigella Sativa Oil ◽  
Total Head ◽  
The Brain

Atorvastatin inhibits brain oxidative stress of Streptozotocininduced diabetic rat

2013 ◽  
Vol 1 (1) ◽  
pp. 35
Author(s):  
Mohammad Taghi Mohammadi ◽  
Mojtaba Gaedniaye Jahromi ◽  
Mohammad Hossein Mirjalili ◽  
Mehdi Ramezani Binabaj ◽  
Mahvash Jafari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Atorvastatin Treatment ◽  
Increase Blood Glucose ◽  
Increase Blood Glucose Level ◽  
Male Wistar Rats ◽  
Brain Oxidative Stress ◽  
The Brain

It is well known that production of ROS compounds and generation of oxidative stress during diabetes are the most important mechanisms of tissue damage. The aim of this study was to examine the effects of atorvastatin treatment, as an antioxidant, to prevent the brain tissue oxidative stress in streptozotocin-induced diabetic rats. Male Wistar rats were randomly divided into four groups (five rats in each group) as followed: normal, normal treated was orally received 20 mg/kg/day atorvastatin for 30 days, diabetic group was given 40 mg/kg streptozotocin by intravenous injection and diabetic treated similar to normal treated rats. After 30 days of treatment, rats were sacrificed under deep anesthesia to remove the brain. After tissue homogenization, superoxide dismutase (SOD) and catalase (CAT) activities, as well as glutathione (GSH) and malondialdehyde (MDA) levels were determined by biochemical methods. In addition to increase blood glucose level in diabetic rats (78%), brain SOD and CAT activities were significantly increased compared with normal rats. Also, diabetes significantly decreased the GSH content of brain tissue by 57%, and increased the brain MDA level by 35%. Finally treatment with atorvastatin significantly decreased the augmented brain CAT activity and the MDA level during diabetes. Based on the finding of this study, diabetes-induced hyperglycemia provoked the production of free radicals in the brain tissue that leading to oxidative stress. Also, treatment with atorvastatin may have prevented from hyperglycemia-induced oxidative stress in the brain of diabetic rat.

scholarly journals Positive effects of angiotensin-converting enzyme (ACE) inhibitor, captopril, on pentylenetetrazole-induced epileptic seizures in mice

2020 ◽  
Vol 19 (3) ◽  
pp. 637-643 ◽  
Author(s):  
Yasar Tastemur ◽  
Erkan Gumus ◽  
Merve Ergul ◽  
Mustafa Ulu ◽  
Recep Akkaya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Converting Enzyme ◽  
Brain Tissue ◽  
Ace Inhibitor ◽  
Neuronal Damage ◽  
Epileptic Seizures ◽  
Neuronal Injury ◽  
Converting Enzyme ◽  
Positive Effects ◽  
The Brain

Purpose: To evaluate the effects of an angiotensin-converting enzyme (ACE) inhibitor, captopril, on pentylenetetrazole (PTZ)-induced seizures and post-seizure hippocampal injury. Materials: Thirty-five male Balb-c mice weighing 30 - 33 g were divided into control, saline PTZ, s(erum physiologic 1 ml/kg as solvent), positive control (valproic acid 200 mg/kg), captopril (25 mg/kg/day for 7 days), and captopril (50 mg/kg/day for 7 days) groups. PTZ (60 mg/kg) was administered thirty minutes after medication administration to induce epileptic seizures. The animals were observed for 30 min to record Racine stages, the time of the first myoclonic jerk (FMJ), and the occurrence of the first generalized tonic-clonic seizure (GTCS). Cornu Ammonis (CA)1, CA2, CA3, and the dentate gyrus (DG) of the hippocampus underwent histopathological examinations. The levels of total oxidant status (TOS), oxidative stress markers (total antioxidant status, TAS), and oxidative stress index (OSI) were measured in the brain tissue. Results: Compared to PTZ group, 25 mg/kg captopril decreased seizure scores and delayed FMJ and GTCS (p < 0.05). Histopathological assessment demonstrated that both 25 and 50 mg/kg captopril alleviated neuronal injury in CA1, CA2, CA3, and DG compared to PTZ (p < 0.05). Also, TOS and OSI levels in the brain tissue were reduced by both 25 and 50 mg/kg doses of captopril (p < 0.05). Conclusion: Captopril favorably improves epileptic seizure parameters and acts against post-seizure neuronal injury in the hippocampus. Captopril may be a drug of choice in epileptic individuals with hypertension. Keywords: Captopril, Angiotensin-converting enzyme, Epilepsy, Pentylenetetrazole, Neuronal damage

scholarly journals CD28 Deficiency Ameliorates Thoracic Blast Exposure-Induced Oxidative Stress and Apoptosis in the Brain through the PI3K/Nrf2/Keap1 Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-14
Author(s):  
Peifang Cong ◽  
Changci Tong ◽  
Ying Liu ◽  
Lin Shi ◽  
Xiuyun Shi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Cytochrome C ◽  
Signaling Pathway ◽  
Brain Tissue ◽  
Caspase 3 ◽  
Histopathological Changes ◽  
Related Factors ◽  
Blast Exposure ◽  
The Brain

Blast exposure is a worldwide public health concern, but most related research has been focused on direct injury. Thoracic blast exposure-induced neurotrauma is a type of indirect injuries where research is lacking. As CD28 stimulates T cell activation and survival and contributes to inflammation initiation, it may play a role in thoracic blast exposure-induced neurotrauma. However, it has not been investigated. To explore the effects of CD28 on thoracic blast exposure-induced brain injury and its potential molecular mechanisms, a mouse model of thoracic blast exposure-induced brain injury was established. Fifty C57BL/6 wild-type (WT) and fifty CD28 knockout (CD28-/-) mice were randomly divided into five groups (one control group and four model groups), with ten mice (from each of the two models) for each group. Lung and brain tissue and serum samples were collected at 12 h, 24 h, 48 h, and 1 week after thoracic blast exposure. Histopathological changes were detected by hematoxylin-eosin staining. The expressions of inflammatory-related factors were detected by ELISA. Oxidative stress in the brain tissue was evaluated by determining the generation of reactive oxygen species (ROS) and the expressions of thioredoxin (TRX), malondialdehyde (MDA), SOD-1, and SOD-2. Apoptosis in the brain tissue was evaluated by TUNEL staining and the levels of Bax, Bcl-xL, Bad, Cytochrome C, and caspase-3. In addition, proteins of related pathways were also studied by western blotting and immunofluorescence. We found that CD28 deficiency significantly reduced thoracic blast exposure-induced histopathological changes and decreased the levels of inflammatory-related factors, including IL-1β, TNF-α, and S100β. In the brain tissue, CD28 deficiency also significantly attenuated thoracic blast exposure-induced generation of ROS and expressions of MDA, TRX, SOD-1, and SOD-2; lowered the number of apoptotic cells and the expression of Bax, cleaved caspase-3, Cytochrome C, and Bad; and maintained Bcl-xL expression. Additionally, CD28 deficiency significantly ameliorated thoracic blast exposure-induced increases of p-PI3K and Keap1 and the decrease of Nrf2 expression in the brain. Our results indicate that CD28 deficiency has a protective effect on thoracic blast exposure-induced brain injury that might be associated with the PI3K/Nrf2/Keap1 signaling pathway.

The beneficial effects of l-cysteine on brain antioxidants of rats affected by sodium valproate

2017 ◽  
Vol 36 (11) ◽  
pp. 1212-1221 ◽  
Author(s):  
RZ Hamza ◽  
NS El-Shenawy
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Protective Effect ◽  
Brain Tissue ◽  
Sodium Valproate ◽  
Histopathological Examination ◽  
Control Group ◽  
High Dose ◽  
Beneficial Effects ◽  
The Brain

Oxidative stress caused by sodium valproate (SV) is known to play a key role in the pathogenesis of brain tissue. The present study was designed to evaluate the protective effect of l-cysteine (LC) on the antioxidants of brain tissue of rats. The animals were divided into six groups: control group 1 was treated with saline as vehicle, groups 2 and 3 were treated with low and high doses of SV (100 and 500 mg/kg, respectively), group 4 was treated with LC (100 mg/kg), and groups 5 and 6 were treated with low-dose SV + LC and high-dose SV + LC, respectively. All the groups were treated orally by gastric tube for 30 successive days. Some antioxidant parameters were determined. Brain tissue (cerebral cortex) of SV-treated animals showed an increase in lipid peroxidation (LPO) and reduction in activity of enzymatic antioxidant and total antioxidant levels. Histopathological examination of cerebral cortex of SV rats showed astrocytic swelling, inflammation, and necrosis. After 4 weeks of the combination treatment of SV and LC daily, results showed significant improvement in the activity of cathepsin marker enzymes and restored the structure of the brain. LC was able to ameliorate oxidative stress deficits observed in SV rats. LC decreased LPO level and was also able to restore the activity of antioxidant enzymes as well as structural deficits observed in the brain of SV animals. The protective effect of LC in SV-treated rats is mediated through attenuation of oxidative stress, suggesting a therapeutic role for LC in individuals treated with SV.

scholarly journals Protective Effect of Hydroalcoholic Extract of Solanum surattense on Brain Tissue Damage and Oxidative Stress in Adult Rats with Toxoplasmosis

2020 ◽  
Vol 1 (1) ◽  
pp. 14-17
Author(s):  
Mansour Ataei ◽  
Arash Khaki ◽  
Yagoob Garedaghi
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Brain Tissue ◽  
Tissue Damage ◽  
Female Rats ◽  
Adult Rats ◽  
Hydroalcoholic Extract ◽  
Solanum Surattense ◽  
Brain Tissue Damage ◽  
The Brain

Introduction: Toxoplasmosis is caused by a protozoan named Toxoplasma gondii. This protozoan is a parasite of cats that can spread among other animals and birds around the world and cause a disease that varies from mild to severe. The disease is seen in the forms of acquired toxoplasmosis and congenital toxoplasmosis. Many studies have shown that there is a relationship between reproductive function and toxoplasmosis. T. gondii has led to decreased reproductive performance of males and females in many experimental animals. The aim of this study was to investigate the protective effect of hydroalcoholic extract of Solanum surattense on the brain tissue damage and brain oxidative stress induced by T. gondii in adult rats. Methods: For this purpose, 32 adult female rats were randomly divided into 4 groups. In group 1, 8 healthy rats received IP saline for 3 weeks. In group 2, 8 rats with T. gondii received IP saline for 3 weeks. In group 3, 8 rats with T. gondii received the hydroalcoholic extract of S. surattense for 3 weeks. In group 4, 8 healthy rats received the hydroalcoholic extract of S. surattense for 3 weeks. Then, brain tissue resection was performed to evaluate histological damage and levels of antioxidant enzymes. Results: Histological and biochemical studies showed that T. gondii had a deleterious effect on the brain tissue of rats and increased the level of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ). The administration of hydroalcoholic extract of S. surattense improved these effects due to its high antioxidant properties. Conclusion: The administration of the appropriate dose of hydroalcoholic extract of S. surattense for three consecutive weeks had a protective effect on brain tissue exposed to T. gondii.

Mechanism of Fisetin Inhibiting Oxidative Stress to Alleviate the Damage of Blood Brain Barrier, Around the Intracerebral Hemorrhag Lesions

2020 ◽  
Vol 10 (6) ◽  
pp. 862-867
Author(s):  
Xinbo Ge ◽  
Qunfu Yang ◽  
Zhenbo Liu ◽  
Tao Zhang ◽  
Chao Liang
Keyword(s):  
Oxidative Stress ◽  
Water Content ◽  
Brain Tissue ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Stress Index ◽  
Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability ◽  
The Brain

Background: The paper determined the brain water content, blood-brain barrier permeability, oxidative stress-related indicators, expressions of tight junction-associated proteins ZO-1 and Occludin, as well as expressions of ERK, p38, and JNK proteins in cerebral hemorrhage rats. The paper explored whether Fisetin reduced the damage of blood-brain barrier caused by cerebral hemorrhage through inhibiting oxidative stress, and investigated whether MAPK pathway is the main pathway for BBB damage caused by oxidative stress. Material and Methods: Rat ICH model was established. After 72 hours, mNSS score was used to measure the behavior of rats. The water content of brain tissue was determined by dry-wet weight method. Evans blue method was applied to measure the blood-brain barrier permeability. Oxidative stress index was detected by spectrophotometer. The expressions of ZO-1, Occludin, ERK, p38 and JNK proteins in rat brain tissue were determined by Western blot. Results: Fisetin significantly reduced the mNSS score, brain water content, bloodbrain barrier permeability, oxidative stress index and the expressions of ERK, p38 and JNK in rat ICH model, and also significantly increased the antioxidant index of rat ICH model, as well as the expressions of ZO-1 and Occludin. The effect is becoming more significant as the therapeutic dose is increased. Conclusion: Fisetin can inhibit the oxidative stress and alleviate the damage of BBB around the lesions of rat ICH model, thus alleviating secondary brain injury. In the rat ICH model, the expressions of ERK, p38 and JNK in the brain tissue around the lesion are increased and oxidized. The stress response is enhanced, and Fisetin inhibits oxidative stress and the expressions of ERK, p38, and JNK. MAPK is imperative in the process of oxidative stress-induced BBB damage in rat ICH model.

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