Methyl jasmonate delays the latency to anoxic convulsions by normalizing the brain levels of oxidative stress biomarkers and serum corticosterone contents in mice with repeated anoxic stress

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Abayomi Ololade Adelaja ◽  
Oluwafemi Gabriel Oluwole ◽  
Oritoke Modupe. Aluko ◽  
Solomon Umukoro
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Methyl Jasmonate ◽  
Brain Injuries ◽  
Antioxidant Property ◽  
Oxidative Stress Biomarkers ◽  
Serum Corticosterone ◽  
Stress Agent ◽  
Cellular Antioxidants ◽  
The Brain

AbstractObjectivesRepeated exposure to anoxic stress damages the brain through cortisol-mediated increases in oxidative stress and cellular-antioxidants depletion. Thus, compounds with antioxidant property might confer protection against anoxic stress-induced brain injuries. In this study, we further examined the protective effect of methyl jasmonate (MJ), a potent anti-stress agent against anoxic stress-induced convulsions in mice.MethodsThirty-six male Swiss mice randomized into six groups (n=6) were given MJ (25, 50 and 100 mg/kg, i.p.) or vehicle (10 mL/kg, i.p.) 30 min before 15 min daily exposure to anoxic stress for 7 days. The latency(s) to anoxic convulsion was recorded on day 7. The blood glucose and serum corticosterone levels were measured afterwards. The brains were also processed for the determination of malondialdehyde, nitrite, and glutathione levels.ResultsMethyl jasmonate (MJ) delayed the latency to anoxic convulsion and reduced the blood glucose and serum corticosterone levels. The increased malondialdehyde and nitrite contents accompanied by decreased glutathione concentrations in mice with anoxic stress were significantly attenuated by MJ.ConclusionsThese findings further showed that MJ possesses anti-stress property via mechanisms relating to the reduction of serum contents of corticosterone and normalization of brain biomarker levels of oxidative stress in mice with anoxic stress.

scholarly journals Reversal of age-associated oxidative stress in mice by PFT, a novel kefir product

2020 ◽  
Vol 34 ◽  
pp. 205873842095014
Author(s):  
Mamdooh Ghoneum ◽  
Shaymaa Abdulmalek ◽  
Deyu Pan
Keyword(s):  
Oxidative Stress ◽  
Low Density Lipoprotein ◽  
Redox Homeostasis ◽  
Density Lipoprotein ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Oxidative Stress Biomarkers ◽  
Age Related ◽  
Total Antioxidant ◽  
The Brain

Introduction: Oxidative stress is a key contributor to aging and age-related diseases. In the present study, we examine the protective effects of PFT, a novel kefir product, against age-associated oxidative stress using aged (10-month-old) mice. Methods: Mice were treated with PFT orally at a daily dose of 2 mg/kg body weight over 6 weeks, and antioxidant status, protein oxidation, and lipid peroxidation were studied in the brain, liver, and blood. Results: PFT supplementation significantly reduced the oxidative stress biomarkers malondialdehyde (MDA) and nitric oxide; reversed the reductions in glutathione (GSH) levels, total antioxidant capacity (TAC), and anti-hydroxyl radical (AHR) content; enhanced the antioxidant enzyme activities of glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD); inhibited the liver enzyme levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT); significantly reduced triglyceride (TG), total cholesterol (TC), and low density lipoprotein (LDL) levels; and significantly elevated high density lipoprotein (HDL) levels. Interestingly, PFT supplementation reversed the oxidative changes associated with aging, thus bringing levels to within the limits of the young control mice in the brain, liver, and blood. We also note that PFT affects the redox homeostasis of young mice and that it is corrected post-treatment with PFT. Conclusion: Our findings show the effectiveness of dietary PFT supplementation in modulating age-associated oxidative stress in mice and motivate further studies of PFT’s effects in reducing age-associated disorders where free radicals and oxidative stress are the major cause.

scholarly journals Lack of mitochondrial ferritin aggravated neurological deficits via enhancing oxidative stress in a traumatic brain injury murine model

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Ligang Wang ◽  
Libo Wang ◽  
Zhibo Dai ◽  
Pei Wu ◽  
Huaizhang Shi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Knockout Mice ◽  
Brain Injuries ◽  
Brain Infarction ◽  
Neurological Deficits ◽  
Important Correlation ◽  
The Brain ◽  
And Oxidative Stress

Oxidative stress has been strongly implicated in the pathogenesis of traumatic brain injury (TBI). Mitochondrial ferritin (Ftmt) is reported to be closely related to oxidative stress. However, whether Ftmt is involved in TBI-induced oxidative stress and neurological deficits remains unknown. In the present study, the controlled cortical impact model was established in wild-type and Ftmt knockout mice as a TBI model. The Ftmt expression, oxidative stress, neurological deficits, and brain injury were measured. We found that Ftmt expression was gradually decreased from 3 to 14 days post-TBI, while oxidative stress was gradually increased, as evidenced by reduced GSH and superoxide dismutase levels and elevated malondialdehyde and nitric oxide levels. Interestingly, the extent of reduced Ftmt expression in the brain was linearly correlated with oxidative stress. Knockout of Ftmt significantly exacerbated TBI-induced oxidative stress, intracerebral hemorrhage, brain infarction, edema, neurological severity score, memory impairment, and neurological deficits. However, all these effects in Ftmt knockout mice were markedly mitigated by pharmacological inhibition of oxidative stress using an antioxidant, N-acetylcysteine. Taken together, these results reveal an important correlation between Ftmt and oxidative stress after TBI. Ftmt deficiency aggravates TBI-induced brain injuries and neurological deficits, which at least partially through increasing oxidative stress levels. Our data suggest that Ftmt may be a promising molecular target for the treatment of TBI.

scholarly journals Experimental Chronic Prostatitis/Chronic Pelvic Pain Syndrome Increases Anxiety-Like Behavior: The Role of Brain Oxidative Stress, Serum Corticosterone, and Hippocampal Parvalbumin-Positive Interneurons

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Nikola Šutulović ◽  
Željko Grubač ◽  
Sonja Šuvakov ◽  
Djurdja Jerotić ◽  
Nela Puškaš ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pelvic Pain ◽  
Chronic Prostatitis ◽  
Chronic Pelvic Pain ◽  
Chronic Pelvic Pain Syndrome ◽  
Pain Syndrome ◽  
Pelvic Pain Syndrome ◽  
Serum Corticosterone ◽  
Brain Oxidative Stress ◽  
The Brain

Mechanisms of the brain-related comorbidities in chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) are still largely unknown, although CP/CPPS is one of the major urological problems in middle-aged men, while these neuropsychological incapacities considerably diminish life quality. The objectives of this study were to assess behavioral patterns in rats with CP/CPPS and to determine whether these patterns depend on alterations in the brain oxidative stress, corticosterone, and hippocampal parvalbumin-positive (PV+) interneurons. Adult male Wistar albino rats from CP/CPPS (intraprostatic injection of 3% λ-carrageenan, day 0) and sham (0.9% NaCl) groups were subjected to pain and anxiety-like behavior tests (days 2, 3, and 7). Afterwards, rats were sacrificed and biochemical and immunohistochemical analyses were performed. Scrotal allodynia and prostatitis were proven in CP/CPPS, but not in sham rats. Ethological tests (open field, elevated plus maze, and light/dark tests) revealed significantly increased anxiety-like behavior in rats with CP/CPPS comparing to their sham-operated mates starting from day 3, and there were significant intercorrelations among parameters of these tests. Increased oxidative stress in the hippocampus, thalamus, and cerebral cortex, as well as increased serum corticosterone levels and decreased number of hippocampal PV+ neurons, was shown in CP/CPPS rats, compared to sham rats. Increased anxiety-like behavior in CP/CPPS rats was significantly correlated with these brain biochemical and hippocampal immunohistochemical alterations. Therefore, the potential mechanisms of observed behavioral alterations in CP/CPPS rats could be the result of an interplay between increased brain oxidative stress, elevated serum corticosterone level, and loss of hippocampal PV+ interneurons.

scholarly journals Methyl Jasmonate Reduces Inflammation and Oxidative Stress in the Brain of Arthritic Rats

Antioxidants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 485 ◽  
Author(s):  
Pereira-Maróstica ◽  
Castro ◽  
Gonçalves ◽  
Silva ◽  
Bracht ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Methyl Jasmonate ◽  
Lipid Peroxides ◽  
Mitochondrial Respiratory Chain ◽  
Antioxidant Defenses ◽  
Protein Carbonyls ◽  
Partial Recovery ◽  
Negative Effects ◽  
The Brain ◽  
And Oxidative Stress

Methyl jasmonate (MeJA), common in the plant kingdom, is capable of reducing articular and hepatic inflammation and oxidative stress in adjuvant-induced arthritic rats. This study investigated the actions of orally administered MeJA (75–300 mg/kg) on inflammation, oxidative stress and selected enzyme activities in the brain of Holtzman rats with adjuvant-induced arthritis. MeJA prevented the arthritis-induced increased levels of nitrites, nitrates, lipid peroxides, protein carbonyls and reactive oxygen species (ROS). It also prevented the enhanced activities of myeloperoxidase and xanthine oxidase. Conversely, the diminished catalase and superoxide dismutase activities and glutathione (GSH) levels caused by arthritis were totally or partially prevented. Furthermore, MeJA increased the activity of the mitochondrial isocitrate dehydrogenase, which helps to supply NADPH for the mitochondrial glutathione cycle, possibly contributing to the partial recovery of the GSH/oxidized glutathione (GSSG) ratio. These positive actions on the antioxidant defenses may counterbalance the effects of MeJA as enhancer of ROS production in the mitochondrial respiratory chain. A negative effect of MeJA is the detachment of hexokinase from the mitochondria, which can potentially impair glucose phosphorylation and metabolism. In overall terms, however, it can be concluded that MeJA attenuates to a considerable extent the negative effects caused by arthritis in terms of inflammation and oxidative stress.

scholarly journals Antioxidant and Astroprotective Effects of aPulicaria incisaInfusion

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Anat Elmann ◽  
Alona Telerman ◽  
Sharon Mordechay ◽  
Hilla Erlank ◽  
Rivka Ofir
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Brain Injuries ◽  
Desert Plant ◽  
Oxygen Species ◽  
Intracellular Accumulation ◽  
Glial Derived Neurotrophic Factor ◽  
The Brain ◽  
Antioxidant Effects

Oxidative stress is involved in the pathogenesis of neurodegenerative diseases such as Parkinson's and Alzheimer's diseases. Astrocytes, the most abundant glial cells in the brain, protect neurons from reactive oxygen species (ROS) and provide them with trophic support, such as glial-derived neurotrophic factor (GDNF). Thus, any damage to astrocytes will affect neuronal survival. In the present study, an infusion prepared from the desert plantPulicaria incisa(Pi) was tested for its protective and antioxidant effects on astrocytes subjected to oxidative stress. ThePiinfusion attenuated the intracellular accumulation of ROS following treatment with hydrogen peroxide and zinc and prevented the H2O2-induced death of astrocytes. ThePiinfusion also exhibited an antioxidant effectin vitroand induced GDNF transcription in astrocytes. It is proposed that thisPiinfusion be further evaluated for use as a functional beverage for the prevention and/or treatment of brain injuries and neurodegenerative diseases in which oxidative stress plays a role.

Evaluation of Prophylactic and Therapeutic Roles of NAcetylcysteine on Biochemical and Oxidative Changes Induced by Acute Poisoning of Diazinon in Various Rat Tissues

2020 ◽  
Vol 14 (2) ◽  
pp. 100-116
Author(s):  
Kavoos Tahmasebi ◽  
Mahvash Jafari ◽  
Farideh Izadi ◽  
Alireza Asgari ◽  
Hoosein Bahadoran ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Biochemical Parameters ◽  
Corn Oil ◽  
Acetylcholinesterase Activity ◽  
Acute Poisoning ◽  
Control Group ◽  
Rat Tissues ◽  
Oxidative Stress Biomarkers ◽  
Male Wistar Rats ◽  
The Brain

Background: Exposure to diazinon (DZN) as an organophosphorus insecticide is associated with reducing the antioxidant capacity of cells. N-acetyl cysteine (NAC) is widely used in clinics to treat several diseases related to oxidative stress. Objective: The current study was aimed to evaluate the prophylactic and therapeutic roles of NAC on biochemical and oxidative changes induced by acute poisoning of DZN in various tissues of male Wistar rats. Methods: Thirty rats were divided into five groups: control group received corn oil as DZN solvent; DZN group received 100 mg/kg of DZN; NAC group received 160 mg/kg of NAC; NAC-DZN and DZN-NAC groups received 160 mg/kg of NAC before and after 100 mg/kg of DZN injection, respectively. Plasma and various tissues were prepared and evaluated for the measurement of the biochemical parameters and oxidative stress biomarkers. Results: Both prophylactic and therapeutic treatments by NAC ameliorated the increased lipid peroxidation and decreased glutathione level and superoxide dismutase, catalase and glutathione S-transferase activities in tissues (P<0.05). Moreover, treatment with the NAC caused a significant reduction in DZN-induced high levels of plasma biochemical parameters. Furthermore, acetylcholinesterase activity was positively correlated with both LDH (P=0.000) activity and GSH (P=0.001) level and negatively correlated with MDA (P=0.009) level in the brain. Conclusion: Results suggest that NAC could effectively ameliorate the DZN-induced oxidative stress and cholinergic hyperactivity in various tissues especially in the brain, through free radicals scavenging and GSH synthesis. Prophylactic approach exerted a stronger protective effect compared to a therapeutic treatment.

scholarly journals STATISTICAL DATA ANALYSIS WHICH RESULT FROM THE BIO-DIAGNOSIS AND BIO-TREATMENT OF INJURED RATS WITH THE HYPERLIPIDEMIA AND HYPERGLYCEMIA DISEASES

2016 ◽  
Vol 9 (9) ◽  
pp. 122
Author(s):  
Hanan Farouk Aly Abduallah ◽  
Howaida I Abdalla ◽  
Sanaa A Ali ◽  
Mohamed M Mamdooh ◽  
Reda Abo Alez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Liver Function ◽  
Blood Glucose Level ◽  
Lipid Profile ◽  
Glucose Level ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
Ipomoea Tricolor ◽  
And Oxidative Stress

ABSTRACTObjective: This study in bioinformatics aims to investigate the potential effect of Ipomoea tricolor and Sophora tomentosa on liver function enzymesactivity, serum lipid profile, oxidative stress biomarkers, and on blood glucose in high fat diet-induced hypercholesterolemia (HC) and STZ-inducedhyperglycemia (HG) in rats.Methods: Blood glucose level, liver function enzymes, alanine aminotransferases and aspartate aminotransferases, alkaline phosphatase, and lactatedehydrogenase (LDH) were determined. Besides, lipid profile including total cholesterol (TC), triacylglycerol (TG), total lipid, and high-densitylipoprotein-cholesterol was investigated. Moreover, oxidative stress biomarkers, lipid peroxide, and nitric oxide as well as non-enzymatic antioxidant,glutathione (GSH) were also examined in different therapeutic groups.Results: A significant increase in blood glucose level, liver function enzyme activities, LDH, lipid profile and oxidative stress markers, while significantdecrease in LDH-C and GSH level in HC-HG induced rats compared to control one. A marked amelioration in all biochemical parameters underinvestigation on treatment of HC-HG rats with I. tricolor and S. tomentosa with different fluctuating percentages of improvement. Histopathologicalexamination of liver and pancreas was also performed and declared HC-HG showed congestion in portal vessels and sinusoids with mild centrilobularhepatocyte degeneration, marked hepatocyte ballooning and hydropic degeneration, while HC-HG treated rats with I. tricolor and S. tomentosa showednormal lobular hepatic architecture with mild sinusoidal dilatation and congestion. On the other hand, a histological organization of pancreas of HC-HGrats showing disarrangement changes in pancreatic blood vessels and interlobular duct as well as disordered in acini. The treatment of HC-HG rats withI. tricolor and S. tomentosa showed enhancement in Langerhans cells and restore of most pancreatic tissue in comparison with standard drugs.Conclusion: The statistical results showed that each extract ameliorated high blood glucose level liver injury, HC and oxidative stress indicatingrelieving of oxidative damage associated with the complexity of HG and HC. These results demonstrated that these two plants extracts may be acandidate intelligent antioxidant, hypolipidemic, hypoglycemic, and hepatoprotective nutraceuticals which need further clinical investigation to beapplied effectively to reduce perturbation in HC associated diabetes.Keywords: Ipomoea tricolor, Sophora tomentosa, Lipid profile and liver function enzymes, Endothelial dysfunction markers, Statistics and imagerecognition, Histopathological analysis.

Comparative study of cholinergic and oxidative stress biomarkers in brains of diabetic and hypercholesterolemic rats

2015 ◽  
Vol 35 (3) ◽  
pp. 251-258 ◽  
Author(s):  
AM Hegazy ◽  
AS Abdel Azeem ◽  
EM Shahy ◽  
EM El-Sayed
Keyword(s):  
Oxidative Stress ◽  
Diabetic Rats ◽  
High Cholesterol Diet ◽  
Iron Level ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
Total Antioxidant ◽  
Increased Activity ◽  
The Brain ◽  
And Oxidative Stress

Objective: Diabetes mellitus (DM) and hypercholesterolemia (HC) when poorly controlled lead to debilitating central nervous system complications including cognitive deficits and memory impairment. In the present study, we investigated the mechanisms that may be responsible for such deficits. Methods: Both diabetes and HC were induced in two groups of rats independently using alloxan and high cholesterol diet, respectively. Results: Acetyl cholinesterase was significantly increased in brain of diabetic rats. Also, brain malondialdehyde level was extremely elevated in both diabetic and hypercholesterolemic groups. Meanwhile, brain albumin was markedly decreased in both of them. However, the brain iron level was significantly increased in DM with concomitant increase in total antioxidant capacity in the same group as compared to the normal control. The concentration of brain calcium was noticeably increased in HC group. Our results were confirmed by the increased activity of lactate dehydrogenase in both DM and HC groups, indicating major brain cytotoxicity. Conclusions: Overall, our results suggested that both DM and HC have deleterious effects on the brain which may be attributed to oxidative stress and dysregulation of both cholinergic function and calcium level. Administration of antioxidant is recommended in both cases.

Sign in / Sign up

Export Citation Format

Share Document