scholarly journals Experimental Brain Injury Induced by Acute Hypobaric Hypoxia Stimulates Changes in mRNA Expression and Stress Marker Status

2021 ◽  
Vol 8 (10) ◽  
pp. 242-247
Author(s):  
Muhammad Shoaib Tahir ◽  
Maged Almezgagi ◽  
Yu Zhang
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Mrna Expression ◽  
Hypobaric Hypoxia ◽  
Male Rats ◽  
Control Group ◽  
Dependent Manner ◽  
Acute Hypobaric Hypoxia ◽  
Time Duration ◽  
The Brain

The present study was proposed to investigate the brain injury under acute hypobaric hypoxia following alteration in mRNA expression and stress markers in a time-dependent manner. SD clean graded male rats were randomly divided into four groups for this experimental brain injury, the control group at Xining (altitude, 2270m) and hypoxia treatment groups with different time exposure day1, day2, and day3 at (altitude, 7000m) in a hypobaric chamber. After day3 exposure, the brain tissues were collected. The level of mRNA expression of VEGF and HIF1-α was assessed using qRT-PCR. The oxidative stress level of superoxide dismutase (SOD) and malondialdehyde (MDA) were determined with commercial kits. AHH with time duration significantly increased the MDA level and decreased in the activity of SOD was seen in all hypoxia treated groups as compared to the control (P< 0.001). The mRNA expression level of HIF1-α and VEGF in day1, day2, and day3 AHH groups was markedly raised when it is compared to control (P< 0.05). Ultimately, in conclusion, such results indicate that AHH stimulates oxidative stress induces brain damage in rats. Keywords: Acute hypobaric hypoxia, Brain injury, HIF-1α, Oxidative stress.

scholarly journals The Effect of Herniarin on Spatial Working Memory, Pain Threshold, and Oxidative Stress in Ischemic Hypoperfusion Model in Rats

2021 ◽  
Vol 7 (1) ◽  
pp. 42-50
Author(s):  
Zahra Nazari Barchestani ◽  
◽  
Maryam Rafieirad ◽  
Keyword(s):  
Oxidative Stress ◽  
Pain Threshold ◽  
Male Rats ◽  
Control Group ◽  
Tail Flick ◽  
Pain Thresholds ◽  
Ischemic Group ◽  
Significant Difference ◽  
The Brain ◽  
And Oxidative Stress

Background: Ischemia causes severe neuronal damage and induces oxidative stress, memory impairment, and reduces pain threshold. Herniarin is a powerful antioxidant. Objectives: This study aimed to evaluate the effect of herniarin on memory, pain, and oxidative stress in an ischemia model in male rats. Materials & Methods: In this study, 50 male rats were divided into 5 groups of control, sham, ischemic, and two other ischemic groups, which received herniarin at doses of 150 and 300 mg/kg by gavage for 14 days. Behavioral tests were performed by shuttle box, and Y-maze and pain tests were performed by Tail-Flick test. Then, the rats’ brains were extracted to evaluate lipid peroxidation and measure the levels of thiol and Glutathione Peroxidase (GPX) in the hippocampus and striatum tissues. The results were expressed as Mean±SEM and then analyzed using suitable statistical methods of ANOVA and least significant difference post-hoc test in SPSS V. 20. Results: Herniarin significantly increased the avoidance memory, spatial memory, and pain thresholds of ischemic rats at different concentrations (P<0.001). Besides, the amount of malondialdehyde (MDA) and thiol in the ischemic group increased significantly in comparison to the control group (P<0.001). Also, in the ischemic group, GPX (P<0.001) significantly decreased. Decreased MDA (P<0.001) and thiol (P<0.001) and increased GPX levels were observed with herniarin administration (P<0.01). Conclusion: According to this study’s results, herniarin can remove free radicals and oxidant substances from the brain. Thus, it improves memory and pain thresholds in the brain hypoperfusion ischemia model.

scholarly journals The possibilities of pharmacological correction of ademol oxidative stress in rates with traumatic brain injury

2021 ◽  
Vol 25 (2) ◽  
pp. 192-195
Author(s):  
S. I. Semenenko
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Brain Injury ◽  
Oxidative Degradation ◽  
Male Rats ◽  
Control Group ◽  
Nacl Solution ◽  
Amantadine Sulfate

Annotation. An important measure of intensive care in patients with traumatic brain injury (TBI) is the use of pharmacotherapeutic agents with antioxidant properties. The aim of this study was to evaluate the effect of ademol compared with amantadine sulfate and 0.9% NaCl solution on the course of oxidative stress in the brain of TBI rats. The experiments were performed on 28 white male rats weighing 160-190 g. The experimental TBI model of severe severity was caused by the action of a carbon dioxide flow under pressure created using a gas balloon pneumatic gun. The therapeutic effect of ademol on model TBI was evaluated with a 2 mg/kg dose. The pseudoperated animals and control group received a 0.9% solution of NaCl and amantadine sulfate at a dose of 2 ml/kg and 5 mg/kg i/v. Data were processed using StatPlus 2009. We used the parametric criterion of t-Student, non-parametric criterion of W. White, paired criterion Ť. Wilcoxon, Fisher's angular transformation at p <0,05. In the course of the experiment, it was found that treatment of rats with TBI ademol leads to a decrease in the activity of lipid peroxidation and oxidative degradation of proteins (p<0.05) and promotes the normalization of the activity of antioxidant enzymes in cells of traumatically damaged brain (p<0.05). The use of ademol compared to amantadine sulfate and 0.9% NaCl solution was accompanied by a more significant decrease in the activity of lipid peroxidation and oxidative degradation of proteins and an improvement in the level of antioxidant enzymes in damaged brain of animals with TBI (p<0.05).

scholarly journals NEURODESTRUCTION OF HYPOTHALAMIC NUCLEI IN BRAIN INJURY. EFFECT OF CARBACETAM

2018 ◽  
Vol 13 (3-4) ◽  
pp. 3-9
Author(s):  
S.V. Ziablitsev ◽  
T.I. Panova ◽  
O.O. Starodubska
Keyword(s):  
Brain Injury ◽  
Nervous Tissue ◽  
Free Fall ◽  
Benzodiazepine Receptor ◽  
Expression Level ◽  
Male Rats ◽  
Control Group ◽  
S 100 ◽  
The Brain ◽  
Supraoptic Nuclei

Relevance. A key role in the pathogenesis of brain injury (BI) is played by destructive changes in the neural tissue of the brain, which consist in damage to neurons and glial cells. To date, various drugs are being intensively developed and studied, which are considered in the perspective of correction and restoration of the functional state of the brain. These substances include the neuroprotector carbacetam, an modulator of the GABA-benzodiazepine receptor complex, a derivative of the alkaloid β-carboline. Objectie. To investigate the effect of carbacetam on neurodestruction processes in the paraventricular and supraoptic nuclei of the hypothalamus in experimental BI. Material and methods. The study was carried out on 20 white non-native male rats weighing 200±10 g. To simulate the BI, rats were subjected to one stroke along the cranial vault with a free-fall load according to the V.N. Yelskyy and S.V. Ziablitsev method (2008). The energy of impact was 0.52 J, the lethality for the first 5 days after injury was 84%. In the control group (n=10) 1 ml of saline was injected intraperitoneally once daily for 10 days after injury. Animals of the experimental group (n=10) received intraperitoneally injections of carbacetam at a dose of 5 mg/kg in 1 ml of saline according to the same scheme. After the experiment was over, the animals were decapitated with the removal of the brain, from which histological preparations were made with a microtome after appropriate histological treatment. Some sections were stained with hematoxylin and eosin, others were immunohistochemically reacted with antibodies against neuronmarkers proteins NSE, S-100 and GFAP. Results. Carbacetam influenced the decrease of degenerative processes in the nervous tissue of the paraventricular and supraoptic nuclei of the hypothalamus. Neurons of animals with BI that received carbacetam, were characterized by the restoration of normal morphological features in contrast to rats not receiving the drug. Immunohistochemical study of brain neuromarkers confirmed the restoration of the functions of neurons and astrocytes in the investigated parts of the rat's hypothalamus after the administration of carbacetam. There was a decrease in the expression level of glial markers GFAP and S-100, which illustrated the decrease in degenerative changes in the nervous tissue. While the expression level of the neuron marker NSE grew, this demonstrated the high metabolic activity of nerve cells. Changes in the expression of markers of neurons and glia indicated a restoration of normal neuronal activity under the action of carbacetam. Conclusion. Further investigation of the effects of carbacetam seems promising in terms of the restoration of neuronal function at BI.

scholarly journals EXPERIMENTAL INVESTIGATION ON CARBACETAM INFLUENCE ON HYPOTHALAMUS TISSUE IN BRAIN INJURY

2018 ◽  
Vol 14 (1-2) ◽  
pp. 11-17
Author(s):  
S.V. Ziablytsev ◽  
T.I. Panova ◽  
O.O. Starodubska ◽  
O.O. Dyadik
Keyword(s):  
Brain Injury ◽  
Physiological Saline ◽  
Neuroendocrine Cells ◽  
Nerve Tissue ◽  
Male Rats ◽  
Control Group ◽  
S 100 ◽  
Hypothalamic Tissue ◽  
Hematoxylin And Eosin ◽  
The Brain

Relevance. A key role in the pathogenesis of the brain injury is played by destructive changes in the hypothalamus neuroendocrine cells. For the correction of such disorders, promising is carbacetam, which has antihypoxic, anti-edema and anti-shock effects. Objective: to investigate the effect of carbacetam on the processes of neurodegeneration in the paraventricular and supraoptical nuclei of the hypothalamus in the experimental brain injury. Material and methods. Brain injury were modeled on the V.M. Elskyy &S.V. Ziablitsev model on white non-breeding male rats weighing 200±10 g. Experimental animals (n=10) received intraabdominal injection of carbacetam at a dose of 5 mg/kg in 1 ml of physiological saline during the seven days after injury. In the control group (n=10), 1 ml of physiological saline was injected. Hypothalamic tissue microparticles performed a morphological and immunohistochemical evaluation of neurodegenerative changes when stained with hematoxylin and eosin and immunohistochemically to detect NSE, S-100 and GFAP neuromarkers. Results. Carbacetam reduced the degenerative processes in the nervous tissue of the paraventricular and supraoptical nuclei of the hypothalamus, which was manifested by the restoration of normal morphological features, in contrast to rats that did not receive the drug. Immunohistochemically, GFAP and S-100 glial markers exhibited reduced, reflecting a reduction in degenerative changes in the nerve tissue. Expressions of the neurons marker NSE increased, reflecting high metabolic activity of the neurons. Conclusions. Revealed changes in the expression of markers of neurons and glia showed a restoration of normal neuronal activity due to the introduction of carbacetam.

scholarly journals Molecular Evidence of the Inhibitory Potential of Melatonin against NaAsO2-Induced Aging in Male Rats

Molecules ◽  
2021 ◽  
Vol 26 (21) ◽  
pp. 6603
Author(s):  
Maryam Baeeri ◽  
Tina Didari ◽  
Madiha Khalid ◽  
Solmaz Mohammadi-Nejad ◽  
Seyed Mojtaba Daghighi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mrna Expression ◽  
Tissue Injury ◽  
High Mobility ◽  
Male Rats ◽  
Control Group ◽  
Molecular Evidence ◽  
Death Domain ◽  
Tissue Samples ◽  
Tnf Α

Arsenic (As) poisoning is widespread due to exposure to pollution. The toxic level of (As) causes oxidative stress-induced aging and tissue damage. Since melatonin (MLT) has anti-oxidant and anti-aging properties, we aimed to evaluate the protective effect of MLT against the toxicity of sodium arsenite (NaAsO2). Healthy male NMRI mice were divided into eight different groups. The control group received a standard regular diet. Other groups were treated with varying diets, including MLT alone, NaAsO2, and NaAsO2 plus MLT. After one month of treatment, biochemical and pathological tests were performed on blood, heart, and lung tissue samples. NaAsO2 increased the levels of TNF-α, 8-hydroxy-2-deoxy guanosine (8OHdG), malondialdehyde (MDA), reactive oxygen species (ROS), and high mobility group box 1 (HMGB1), increased the expression of TNF receptor type 1-associated death domain (TRADD) mRNA and telomerase reverse transcriptase, and decreased the expression of Klotho (KL) mRNA in both plasma and tissues. In contrast, MLT reduced MDA, ROS, HMGB1, lactate, and TNF-α enhanced the mRNA expression of KL, and suppressed the mRNA expression of the TERT and TRADD genes. Thus, MLT confers potent protection against NaAsO2- induced tissue injury and oxidative stress.

The effects of crocin (active contstituent of saffron) treatment on brain antioxidant enzyme mRNA levels in diabetic rats / Diyabetik ratlarda safranın aktif içeriği olan krosin tedavisinin beyindeki antioksidan enzimlerin mRNA seviyeleri üzerine etkisi

2016 ◽  
Vol 41 (2) ◽  
Author(s):  
Eyüp Altınöz ◽  
Cemal Ekici ◽  
Berna Özyazgan ◽  
Yılmaz Çiğremiş
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Mrna Expression ◽  
Antioxidant Enzyme ◽  
Diabetic Rats ◽  
Control Group ◽  
Mrna Levels ◽  
The Brain ◽  
And Oxidative Stress

AbstractObjective: The aim of the present study is to evaluate the effect of crocin on mRNA expression of antioxidant enzymes, SOD, CAT and GPX in the brain of the STZ induced diabetic rats.Methods: Thirty animals randomized in three groups containing ten animals in each group as follows; control (non-diabetic rats), DM (STZ-induced untreated diabetic rats), DM+crocin (STZ-induced diabetic rats treated with crocin,). Crocin was given at a dose of 20 mg/kg bw/day by gavage for 21 days.Results: STZ injection caused a significant increase in mRNA expression of antioxidant enzymes, SOD, CAT and GPX when compared to control group. Crocin given to diabetic rats significantly decreased mRNA expression of antioxidant enzymes, SOD, CAT and GPX when compared to DM group.Conclusion: The present study demonstrates that crocin can modulate mRNA expression of antioxidant enzymes, SOD, CAT and GPX and oxidative stress in the brain of the STZ induced diabetic rats.

scholarly journals EXPERIMENTAL INVESTIGATION ON CARBACETAM INFLUENCE ON HYPOTHALAMUS TISSUE IN BRAIN INJURY

2018 ◽  
Vol 14 (1-2) ◽  
pp. 11-17 ◽  
Author(s):  
S.V. Ziablytsev ◽  
T.I. Panova ◽  
O.O. Starodubska ◽  
O.O. Dyadik
Keyword(s):  
Brain Injury ◽  
Physiological Saline ◽  
Neuroendocrine Cells ◽  
Nerve Tissue ◽  
Male Rats ◽  
Control Group ◽  
S 100 ◽  
Hypothalamic Tissue ◽  
Hematoxylin And Eosin ◽  
The Brain

Relevance. A key role in the pathogenesis of the brain injury is played by destructive changes in the hypothalamus neuroendocrine cells. For the correction of such disorders, promising is carbacetam, which has antihypoxic, anti-edema and anti-shock effects. Objective: to investigate the effect of carbacetam on the processes of neurodegeneration in the paraventricular and supraoptical nuclei of the hypothalamus in the experimental brain injury. Material and methods. Brain injury were modeled on the V.M. Elskyy &S.V. Ziablitsev model on white non-breeding male rats weighing 200±10 g. Experimental animals (n=10) received intraabdominal injection of carbacetam at a dose of 5 mg/kg in 1 ml of physiological saline during the seven days after injury. In the control group (n=10), 1 ml of physiological saline was injected. Hypothalamic tissue microparticles performed a morphological and immunohistochemical evaluation of neurodegenerative changes when stained with hematoxylin and eosin and immunohistochemically to detect NSE, S-100 and GFAP neuromarkers. Results. Carbacetam reduced the degenerative processes in the nervous tissue of the paraventricular and supraoptical nuclei of the hypothalamus, which was manifested by the restoration of normal morphological features, in contrast to rats that did not receive the drug. Immunohistochemically, GFAP and S-100 glial markers exhibited reduced, reflecting a reduction in degenerative changes in the nerve tissue. Expressions of the neurons marker NSE increased, reflecting high metabolic activity of the neurons. Conclusions. Revealed changes in the expression of markers of neurons and glia showed a restoration of normal neuronal activity due to the introduction of carbacetam.

Chronic immobilization stress induces anxiety-related behaviors and affects brain essential minerals in male rats

2020 ◽  
pp. 1-8
Author(s):  
Zafer Sahin ◽  
Alpaslan Ozkurkculer ◽  
Omer Faruk Kalkan ◽  
Ahmet Ozkaya ◽  
Aynur Koc ◽  
...  
Keyword(s):  
Immobilization Stress ◽  
Central Area ◽  
Essential Elements ◽  
Male Rats ◽  
Control Group ◽  
Male Wistar Rats ◽  
Swimming Test ◽  
The Brain ◽  
Center Area ◽  
Chronic Immobilization Stress

Abstract. Alterations of essential elements in the brain are associated with the pathophysiology of many neuropsychiatric disorders. It is known that chronic/overwhelming stress may cause some anxiety and/or depression. We aimed to investigate the effects of two different chronic immobilization stress protocols on anxiety-related behaviors and brain minerals. Adult male Wistar rats were divided into 3 groups as follows ( n = 10/group): control, immobilization stress-1 (45 minutes daily for 7-day) and immobilization stress-2 (45 minutes twice a day for 7-day). Stress-related behaviors were evaluated by open field test and forced swimming test. In the immobilization stress-1 and immobilization stress-2 groups, percentage of time spent in the central area (6.38 ± 0.41% and 6.28 ± 1.03% respectively, p < 0.05) and rearing frequency (2.75 ± 0.41 and 3.85 ± 0.46, p < 0.01 and p < 0.05, respectively) were lower, latency to center area (49.11 ± 5.87 s and 44.92 ± 8.04 s, p < 0.01 and p < 0.01, respectively), were higher than the control group (8.65 ± 0.49%, 5.37 ± 0.44 and 15.3 ± 3.32 s, respectively). In the immobilization stress-1 group, zinc (12.65 ± 0.1 ppm, p < 0.001), magnesium (170.4 ± 1.7 ppm, p < 0.005) and phosphate (2.76 ± 0.1 ppm, p < 0.05) levels were lower than the control group (13.87 ± 0.16 ppm, 179.31 ± 1.87 ppm and 3.11 ± 0.06 ppm, respectively). In the immobilization stress-2 group, magnesium (171.56 ± 1.87 ppm, p < 0.05), phosphate (2.44 ± 0.07 ppm, p < 0.001) levels were lower, and manganese (373.68 ± 5.76 ppb, p < 0.001) and copper (2.79 ± 0.15 ppm, p < 0.05) levels were higher than the control group (179.31 ± 1.87 ppm, 3.11 ± 0.06 ppm, 327.25 ± 8.35 ppb and 2.45 ± 0.05 ppm, respectively). Our results indicated that 7-day chronic immobilization stress increased anxiety-related behaviors in both stress groups. Zinc, magnesium, phosphate, copper and manganese levels were affected in the brain.

Effect of Turmeric and Ginger on Lipid Profile in Male Rats Exposed to Oxidative Stress

2019 ◽  
Vol 10 (01) ◽  
Author(s):  
Eman A. Al-Rekabi ◽  
Dheyaa K. Alomer ◽  
Rana Talib Al-Muswie ◽  
Khalid G. Al-Fartosi
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Drinking Water ◽  
Lipid Profile ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Male Rats ◽  
Control Group ◽  
Very Low Density Lipoprotein ◽  
Low Density

The present study aimed to investigate the effect of turmeric and ginger on lipid profile of male rats exposed to oxidative stress induced by hydrogen peroxide H2O2 at a concentration of 1% given with consumed drinking water to male rats. Methods: 200 mg/kg from turmeric and ginger were used, and the animals were treatment for 30 days. Results: the results showed a significant increase in cholesterol, triglycerides, low density lipoprotein (LDL), very low density lipoprotein (VLDL), whereas it explained a significant decrease in high density lipoprotein (HDL) of male rats exposed to oxidative stress when compared with control group. the results showed a significant decrease in cholesterol, triglycerides, (LDL), (VLDL), whereas it explained a significant increase in (HDL) of rats treated with turmeric and ginger at dose 200 mg/kg when compared with male rats exposed to oxidative stress.

Effect of Opuntia dejecta (Salm-Dyck) flowers in liver of fructose-fed rats: Biochemicals, enzymatic and histological studies

2021 ◽  
pp. 096032712110134
Author(s):  
O Zouaoui ◽  
K Adouni ◽  
A Jelled ◽  
A Thouri ◽  
A Ben Chrifa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Body Weight ◽  
Diabetes Type 2 ◽  
Male Rats ◽  
Control Group ◽  
Standard Drug ◽  
High Fructose ◽  
Group A ◽  
Histological Architecture

Phytochemical composition and antioxidant activity of flowers decoction at post-flowering stage (F3D) of Opuntia dejecta were determined. The obtained findings demonstrate that F3D has a marked antioxidant activity in all tested assays. Furthermore, the present study was designed to test the protective activity of F3D against induced Diabetes type 2 (DT2) in male rats. Those metabolic syndromes were induced by a high-fructose diet (HFD) (10% fructose solution) for a period of 20 weeks. F3D was administered orally (100 and 300 mg/kg body weight) daily for the last 4 weeks. Metformin (150 mg/kg body weight) was used as a standard drug and administrated orally for the last 4 weeks. The results showed a significant increase in blood glucose, triglycerides and hepatic markers (ALAT, ASAT and ALK-P) in HFD group. A significant increase in hepatic TBARS and a significant decrease in SOD, CAT and GPX were observed in fructose fed rats compared to control group. Administration of F3D showed a protective effect in biochemical and oxidative stress parameters measured in this study. Also, oral administration of F3D restored the histological architecture of rat liver in comparison with rats fed HFD. In conclusion, F3D attenuated hepatic oxidative stress in fructose-fed rats.

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