scholarly journals Medicinal Plants Extracts Impact on Oxidative Stress in Mice Brain under the Physiological Conditions: the Effects of Corn Silk, Parsley, and Bearberry

2021 ◽  
Vol 68 (4) ◽  
pp. 896-903
Author(s):  
Marijana Vranješ ◽  
Dubravka Štajner ◽  
Dejan Vranješ ◽  
Bojana Blagojević ◽  
Ksenija Pavlović ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
Control Level ◽  
Biological Properties ◽  
Physiological Conditions ◽  
Corn Silk ◽  
Medicinal Plant Extracts ◽  
Mice Brain ◽  
Radical Content ◽  
The Brain

This study was performed to examine the effects of medicinal plant extracts of corn silk (Stigma maydis), parsley leaf (Petroselini folium), and bearberry leaf (Uvae ursi folium) on antioxidant status of the brain of experimental animals (mice) under the physiological conditions. Biological properties of these plants are insufficiently investigated and the aim was to explore their possible antioxidant effects that can alleviate oxidative damage of the brain tissue. Corn silk extract showed positive effect on activities of antioxidant enzymes in mice brain tissue. Parsley extract induced the increase in glutathione content and decrease of lipid peroxidation. Bearberry leaf extract induced catalase activity and decrease of hydroxyl radical content, while malonyldialdehide accumulation was maintained at the control level. Results obtained in this study support the use of corn silk, parsley and bearberry leaves as natural antioxidant sources in the prevention and treatment of brain tissue damages and different diseases caused by oxidative stress.

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.

Neurochemical effects of choline supplementation

1986 ◽  
Vol 64 (3) ◽  
pp. 329-333 ◽  
Author(s):  
Lynn Wecker
Keyword(s):  
Brain Tissue ◽  
Neuronal Activity ◽  
Cholinergic Neurons ◽  
Lipid Phosphorus ◽  
Drug Induced ◽  
Pharmacological Agents ◽  
Physiological Conditions ◽  
Free Choline ◽  
Drug Challenge ◽  
The Brain

Whether or not the brain can use supplemental choline to enhance the synthesis of acetylcholine (ACh) is an important consideration for assessing the merits of using choline or phosphatidylcholine (lecithin) for the treatment of neuropsychiatric disorders postulated to involve hypocholinergic activity. While it is well documented that administered choline is incorporated into ACh, the ability of supplemental choline to increase the synthesis and release of ACh has been questionable. Studies in my laboratory have demonstrated that acute or chronic choline supplementation does not, by itself, enhance the levels of ACh in brain under normal biochemical and physiological conditions. However, supplemental choline prevents the depletion of ACh in brain induced by numerous pharmacological agents that increase the firing of cholinergic neurons. Since the levels of free choline in brains from supplemented rats were not different from controls prior to drug challenge, evidence suggested that the observed effects of choline were mediated by alterations in the mobilization of choline from choline-containing compounds. Studies investigating the release of choline from brain indicated that more choline was released per unit time in tissues from choline-supplemented rats than from controls. In addition, brain tissue from choline-supplemented rats had increased concentrations of total lipid phosphorus as compared with controls. Hence, although choline supplementation does not alter the levels of ACh in brain under normal conditions, it does appear to support ACh synthesis during drug-induced increases in neuronal activity, an effect most likely mediated by alterations in the metabolism of choline-containing phospholipids.

scholarly journals Natural Compounds Rosmarinic Acid and Carvacrol Counteract Aluminium-Induced Oxidative Stress

Molecules ◽  
2020 ◽  
Vol 25 (8) ◽  
pp. 1807 ◽  
Author(s):  
Juste Baranauskaite ◽  
Ilona Sadauskiene ◽  
Arunas Liekis ◽  
Arturas Kasauskas ◽  
Robertas Lazauskas ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Phenolic Compounds ◽  
Rosmarinic Acid ◽  
Sod Activity ◽  
Mice Brain ◽  
Aluminum Accumulation ◽  
Liver Homogenates ◽  
The Brain

Aluminum accumulation, glutathione (GSH) and malondialdehyde (MDA) concentrations as well as catalase (CAT) and superoxide dismutase (SOD) activities were determined in erythrocytes and brain and liver homogenates of BALB/c mice treated with Al3+ (7.5 mg/kg/day (0.15 LD50) as AlCl3 (37.08 mg/kg/day), whereas HCl (30.41 mg/kg/day) was used as Cl− control, the treatments were performed for 21 days, i.p., in the presence and absence of rosmarinic acid (0.2805 mg/kg/day (0.05 LD50), 21 days, i.g.) or carvacrol (0.0405 mg/kg/day (0.05 LD50), 21 days, i.g.). The treatment with AlCl3 increased GSH concentration in erythrocytes only slightly and had no effect on brain and liver homogenates. Rosmarinic acid and carvacrol strongly increased GSH concentration in erythrocytes but decreased it in brain and liver homogenates. However, AlCl3 treatment led to Al accumulation in mice blood, brain, and liver and induced oxidative stress, assessed based on MDA concentration in the brain and liver. Both rosmarinic acid and carvacrol were able to counteract the negative Al effect by decreasing its accumulation and protecting tissues from lipid peroxidation. AlCl3 treatment increased CAT activity in mice brain and liver homogenates, whereas the administration of either rosmarinic acid or carvacrol alone or in combination with AlCl3 had no significant effect on CAT activity. SOD activity remained unchanged after all the treatments in our study. We propose that natural herbal phenolic compounds rosmarinic acid and carvacrol could be used to protect brain and liver against aluminum induced oxidative stress leading to lipid peroxidation.

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.

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