scholarly journals Rosinidin Attenuates Lipopolysaccharide-Induced Memory Impairment in Rats: Possible Mechanisms of Action Include Antioxidant and Anti-Inflammatory Effects

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1747
Author(s):  
Sultan Alshehri ◽  
Syed Sarim Imam
Keyword(s):  
Oxidative Stress ◽  
Locomotor Activity ◽  
Memory Impairment ◽  
Spontaneous Locomotor Activity ◽  
Oxidative Stress Marker ◽  
Vehicle Group ◽  
Treatment Schedule ◽  
Learning Abilities ◽  
Tnf Α ◽  
Group 1

The investigation aimed to evaluate the favourable effects of rosinidin in lipopolysaccharide (LPS)-induced learning and memory impairment in rats. Adult Wistar rats (150–200 g) were segregated equally into four different groups and treated as below: Group 1 (normal) and Group 2 (LPS control) were administered orally with 3 mL of 0.5% SCMC (vehicle); Group 3 and Group 4 were test groups and orally administered with rosinidin lower dose (10 mg/kg) and higher dose 20 mg/kg. Daily, 1 h post-offer mentioned treatments, Group 1 animals were injected with normal saline (i.p.) and groups 2–4 were treated with 1 mg/kg/day of LPS. This treatment schedule was followed daily for 7 days. During the treatment, schedule rats were evaluated for spontaneous locomotor activity, memory, and learning abilities. The biochemical assessment was carried out of acetylcholine esterase (AChE), endogenous antioxidants (GSH, SOD, GPx, and catalase), oxidative stress marker MDA, neuroinflammatory markers (IL-6, IL-1β, TNF-α, and NF-κB), and BDNF. LPS-induced reduced spontaneous locomotor activity and memory impairment in the animals. Moreover, LPS reduced GSH, SOD, GPx, and catalase levels; altered activities of AChE; elevated levels of MDA, IL-6, IL-1β, TNF-α, and NF-κB; and attenuated the levels of BDNF in brain tissue. Administration of rosinidin to LPS-treated animals significantly reduced LPS-induced neurobehavioral impairments, oxidative stress, neuroinflammatory markers, and reversed the Ach enzyme activities and BDNF levels towards normal. Results demonstrated that rosinidin attenuates the effects of LPS on learning memory in rats.

scholarly journals Effect of treatment with trypanocides on Trypanosoma brucei induced oxidative stress and antioxidant enzyme activities in dogs

2021 ◽  
Vol 19 (2) ◽  
pp. 121-128
Author(s):  
P.O. Akpa ◽  
P.U. Umeakuana ◽  
T.O. Nnaji ◽  
B.M. Anene
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Trypanosoma Brucei ◽  
Post Infection ◽  
Oxidative Stress Marker ◽  
Antioxidant Enzyme Activities ◽  
Pathophysiological Mechanism ◽  
Group 4 ◽  
Group 2 ◽  
Group 1

Oxidative stress and alteration of endogenous antioxidant enzymes play roles in the pathophysiological mechanism of trypanosomosis. The oxidative stress marker: malondialdehyde- MDA and antioxidative stress markers: Serum catalase- CAT, Serum Reduced Glutathione -GSH-Rd and Serum Superoxide dismutase- SOD of Nigerian local dogs (NLD) experimentally infected with Trypanosoma brucei were evaluated after treatments with diminazene aceturate (DA) and isometamidium chloride (IMC). Twenty dogs of age 3 – 4 months were assigned to any of the four groups of five dogs each as follows: 1 = infected and treated with DA (7.0 mg/kg); 2 = uninfected untreated; 3 = infected and untreated; 4 = infected and treated with IMC (0.5 mg/kg). DA and IMC cleared the parasites from the blood, following treatment of the dogs. Relapse was recorded in two dogs in group 1 and one dog in group 4 on days 35 and 56 post-infection (PI) respectively. No dog died except one in group 1. The levels of malondialdehyde- MDA increased significantly by day 7 post-infection in all the infected groups. However, by day 14 post-infection the malondialdehyde levels in group 4 became similar with group 2. The MDA level in group 1 remained significantly higher than in group 2. As from days 7 – 14 post-infection Catalase, Reducedg glutathionend superoxide dismutase levels in the infected groups were significantly lower than group 2. Nevertheless, both trypanocides did not return the levels of CAT, GSH, and SOD to pre-infection values before the termination of the experiment. The findings suggested that the two trypanocides could neither reverse the induced oxidative stress nor normalize the antioxidant capacity of the dogs infected with T. brucei.

Etanercept Improves Lipid Profile and Oxidative Stress Measures in Patients with Juvenile Idiopathic Arthritis

2013 ◽  
Vol 40 (6) ◽  
pp. 943-948 ◽  
Author(s):  
Sara De Sanctis ◽  
M. Loredana Marcovecchio ◽  
Stefania Gaspari ◽  
Marianna Del Torto ◽  
Angelika Mohn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Juvenile Idiopathic Arthritis ◽  
Disease Activity ◽  
Lipid Profile ◽  
Proinflammatory Cytokines ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Oxidative Stress Marker ◽  
Tnf Α ◽  
And Oxidative Stress

Objective.To investigate the effect of 1-year treatment with the anti-tumor necrosis factor-α (TNF-α) drug etanercept on lipid profile and oxidative stress in children and adolescents with juvenile idiopathic arthritis (JIA).Methods.Thirty children with JIA (22 females; mean age 12.3 ± SD 5.7 yrs), all eligible for anti-TNF-α treatment, were assessed at baseline and after 6- and 12-month treatment with etanercept. Disease activity was determined using the Juvenile Arthritis Disease Activity Score (JADAS). Blood samples were drawn to measure the acute-phase reactants C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), lipids, and the proinflammatory cytokines TNF-α, interleukin-1β (IL-1β), IL-6 and interferon-γ. To measure the oxidative stress marker 8-iso-prostaglandin F2α, 24-h urine samples were collected.Results.Inflammatory indicators (CRP and ESR) and JADAS scores improved significantly after 1 year of etanercept treatment (all p < 0.001). Proinflammatory cytokines showed significant reduction during the study period (all p < 0.001). Similar reductions were detected in total cholesterol (p < 0.001), low-density lipoprotein cholesterol (p = 0.04), and triglycerides (p < 0.001), whereas no significant change was found in high-density lipoprotein cholesterol. No side effects were observed during the treatment period.Conclusion.This study shows for the first time that anti-TNF-α therapy for JIA is associated not only with a beneficial effect on clinical disease activity and inflammatory indexes, but also with improved lipid profile and oxidative stress. These findings suggest that TNF-α blockers might reduce atherosclerotic risk in children with JIA.

scholarly journals Influence of TNF-α inhibition on oxidative stress of rheumatoid arthritis patients

Reumatismo ◽  
2016 ◽  
Vol 67 (3) ◽  
pp. 97 ◽  
Author(s):  
F. Cacciapaglia ◽  
M.G. Anelli ◽  
D. Rizzo ◽  
E. Morelli ◽  
C. Scioscia ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Health Assessment ◽  
Good Control ◽  
Oxidative Stress Marker ◽  
Reactive Oxygen Metabolites ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Tnf Α ◽  
Oxidative Stress Status

The aim of this study was to assess circulating levels of reactive oxygen metabolites (ROMs) as a marker of oxidative stress in rheumatoid arthritis (RA) patients during an anti-tumor necrosis factor alpha (TNF-α) treatment. We enrolled 40 patients with RA (36 females; age 53±13 yrs) treated with different subcutaneously administered TNF-α inhibitors. The oxidative status was determined on the basis of plasma samples taken before, at 24 and 52 weeks of the anti-TNF-α treatment. Hydroperoxide levels were measured using the d-ROMs test, a useful clinically proven oxidative stress marker. During the anti-TNF-α therapy, we observed a significant reduction in serum ROMs levels in RA patients from 33.2±10 mg H2O2/L at baseline to 29.5±7 and 29.3±9 mg H2O2/L, at 24 and 52 weeks, respectively (p&lt;0.05). We also identified a significant correlation between the oxidative stress status and the disease activity score on 28 joints/C-reactive protein and health assessment questionnaire disability index. The results of our study demonstrate that a good control of the disease with anti-TNF-α agents can reduce oxidative stress in RA patients. However, further studies of larger patient cohorts are needed to confirm these preliminary data.

scholarly journals D-galactose induced dysfunction in mice hippocampus and the possible antioxidant and neuro-modulatory effects of selenium

2021 ◽  
Author(s):  
Noreen Samad ◽  
Farheen Hafeez ◽  
Imran Imran
Keyword(s):  
Oxidative Stress ◽  
Memory Impairment ◽  
Oxidative Stress Marker ◽  
Repeated Treatment ◽  
Neurochemical Analysis ◽  
Repeated Doses ◽  
Behavioural Tests ◽  
Neuro Protection ◽  
Anxiety Depression ◽  
The Brain

Abstract Aging is an ultimate reality that everyone has to face. D-galactose (D-gal) has been used extensively to develop aging model. Trace elements such as selenium (Sel) have been used as a potential antioxidant for neuro-protection. The present work aims to develop therapeutic agents such as Sel for the treatment of aging-induced neurological ailments such as anxiety, depression, and memory impairment. For this purpose, mice were treated with D-gal at a dose of 300 mg/ml/kg and various doses of Sel (0.175 and 0.35mg/ml/kg) for 28 days. Behavioural tests were monitored after treatment days. After the behavioural assessment mice were decapitated and their brains were collected. Hippocampi were removed from the brain for biochemical and neurochemical analysis. The present findings of behavioural analysis showed that D-gal induced anxiety and depression-like symptoms were inhibited by both doses of Sel. D-gal induced memory alteration was also prevented by repeated doses (0.175 and 0.35mg/ml/kg) of Sel. Biochemical analysis showed that D-gal induced increase of oxidative stress marker and decrease of antioxidant enzymes in the hippocampus was prevented by Sel administration. An increase in the activity of acetylcholinesterase was also diminished by Sel. The neurochemical assessment showed that D-gal induced increased serotonin metabolism and decreased acetylcholine levels in the hippocampus were restored by repeated treatment of Sel. It is concluded that D-gal induced dysfunction in mice hippocampus caused anxiety, depression, memory impairment, oxidative stress that were mitigated by Sel via its antioxidant potential and modulating capability of serotonergic and cholinergic functions.

scholarly journals Peculiarities of the influence of antihypertensive therapy on endothelial function, oxidative stress and immune activation in obese patients

2017 ◽  
Vol 8 (2) ◽  
pp. 152-156 ◽  
Author(s):  
T. V. Ashcheulova ◽  
N. N. Gerasimchuk
Keyword(s):  
Oxidative Stress ◽  
Endothelial Function ◽  
Antihypertensive Therapy ◽  
Overweight And Obesity ◽  
Oxidative Stress Marker ◽  
Control Group ◽  
Type I ◽  
Soluble Receptor ◽  
Hypertensive Patients ◽  
Tnf Α

This article aims to improve combined antihypertensive therapy on the basis of studying the antioxidant properties of bisoprolol and indapamid, their impact on endothelial dysfunction (ED) and pro-inflammatory cytokines activity in hypertensive patients with overweight and obesity. A combination of a β-blocker (BAB) with a diuretic (D) (bisoprolol 2.5, 5, 10 mg and indapamid 1.5–2.5 mg/day) was prescribed to 102 patients with essential hypertension of 1–3 grades, 30 to 65 years old (mean age – 54.54 ± 0.91 years), who previously had not been receiving regular antihypertensive therapy. The daily dose of bisoprolol was administered by continuous slow titration, starting with low doses of 1.25 mg/day. Of the patients 82 were women and 20 men, the duration of disease averaged 9.0 ± 0.71 years. The control group included 16 healthy subjects matched for age and sex. The level of stable terminal metabolites of nitric oxide NO (nitrite NO2– and nitrate NO3–), the concentration of S-nitrosothiol and NO-synthases (NOS), SOD, and catalase activity was determined biochemically. The contents of serum 8-iso-PgF2α (8-isoprostane), TNF-alpha and its type I soluble receptor (sTNF-αRI) were determined in all subjects using the “8-isoprostane ELISA” (Usbiological,USA), “ProCon TNFα” (ProteinContour,Russian Federation) and “sTNF-RI EASIA” (BioSource Europe SA,Belgium) ELISA kits, respectively. During the course of combined antihypertensive therapy we observed a significant decrease of S-nitrosothiols levels, i-NOS activity, reduction of TNF-α type I of its soluble receptor (sTNF-αRI), and oxidative stress marker – 8-iso-PgF2α in the examined patients. Nitrites and nitrates serum levels, activity of e-NOS, superoxide dismutase and catalase, by contrast, were increased in patients with hypertension and concomitant obesity. These changes may reflect the fact that against the background of the therapy there was a reduction in tension of oxidative stress, which leads to an improvement in endothelial function. Significant reduction ratio of TNF-α/sTNF-αRI shows suppression of autoimmune and apoptotic activity in patients under treatment. Thus, the improvement of endothelial function, a significant decrease in autoimmune activation due to lower tension of oxidative stress in the examined patients optimizes use of a combination of bisoprolol and indapamid for differentiated therapy in hypertensive patients with obesity. 

scholarly journals Ellagic Acid Alleviates Rheumatoid Arthritis in Rats through Inhibiting MTA1/HDAC1-Mediated Nur77 Deacetylation

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Huanjin Song ◽  
Hao Wu ◽  
Jun Dong ◽  
Sihua Huang ◽  
Jintao Ye ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Ellagic Acid ◽  
Oxidative Stress Marker ◽  
Dependent Manner ◽  
Histone Deacetylase 1 ◽  
Protein Levels ◽  
Tnf Α ◽  
And Oxidative Stress

Ellagic acid (EA) was reported to play protective roles in rheumatoid arthritis (RA). It was found that the level of metastasis-associated gene 1 (MTA1)/histone deacetylase 1 (HDAC1) protein complex was downregulated by polyphenols in several human disorders. Notably, inhibition of MTA1 or HDAC1 has anti-inflammatory effects on RA. Therefore, our study is aimed at investigating whether EA prevents RA progression through regulating the MTA1/HDAC1 complex. Herein, the human fibroblast-like synoviocyte (FLS) cell line MH7A was treated with TNF-α to induce an inflammation model in vitro and then incubated with different concentrations of EA. Western blot analysis showed that EA reduced MTA1 expression in a dose-dependent manner in MH7A cells. Then, TNF-α-treated MH7A cells were incubated with EA alone or together with MTA1 overexpression plasmid (pcDNA-MTA1), and we found that EA inhibited proliferation, inflammation cytokine levels, and oxidative stress marker protein levels and promoted apoptosis in MH7A cells, while MTA1 overexpression abolished these effects. Moreover, coimmunoprecipitation assay verified the interaction between MTA1 and HDAC1. EA downregulated the MTA1/HDAC1 complex in MH7A cells. MTA1 knockdown inhibited proliferation, inflammation, and oxidative stress and promoted apoptosis in MH7A cells, while HDAC1 overexpression reversed these effects. Moreover, chromatin immunoprecipitation assay indicated that EA inhibited HDAC1-mediated Nur77 deacetylation. Rescue experiments demonstrated that Nur77 knockdown reversed the effects of EA on MH7A cell biological behaviors. Additionally, EA treatment attenuated arthritis index, paw swelling, synovial hyperplasia, and inflammation in collagen-induced arthritis (CIA) rats. In conclusion, EA inhibited proliferation, inflammation, and oxidative stress and promoted apoptosis in MH7A cells and alleviated the severity of RA in CIA rats though downregulating MTA1/HDAC1 complex and promoting HDAC1 deacetylation-mediated Nur77 expression.

High-dose testosterone and dehydroepiandrosterone induce cardiotoxicity in rats

2015 ◽  
Vol 35 (5) ◽  
pp. 562-572 ◽  
Author(s):  
E Emer ◽  
O Yildiz ◽  
M Seyrek ◽  
S Demirkol ◽  
T Topal ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Locomotor Activity ◽  
Muscle Strength ◽  
Left Ventricular ◽  
Oxidative Stress Marker ◽  
High Dose ◽  
Cell Nuclei ◽  
Myocardial Fibers ◽  
The Impact

The aim of this study is to assess cardiotoxic effect of testosterone (TES) and dehydroepiandrosterone (DHEA) in Sprague Dawley rats. We compared the impact of subacute (14 days) and subchronic (90 days) administration of suprapharmacologic doses of TES and DHEA on body weight, locomotor activity, muscle strength, echocardiographic parameters, heart histopathology, and oxidative stress markers with the control group. Testosterone (10, 30, and 100 mg/100 g body weight) and DHEA (10 mg/100 g body weight) administration decreased the body weights and locomotor activity ( p < 0.05), and the combination of both increased muscle strength ( p < 0.05) in rats. In our histopathological evaluation, misshapen cell nuclei, disorganized myocardial fibers, and leukocytic infiltrates were observed in high-dose TES (100 mg/100 g)-treated rats, especially on day 14. On day 90, mild changes such as misshapen cell nuclei, disorganized myocardial fibers, and leukocytic infiltrates were observed in TES and DHEA-treated groups. According to our echocardiographic study on day 14 and day 90, TES, especially at high doses, induced increase in left ventricular posterior wall diameter and ejection fraction ( p < 0.05). In this study, blood oxidative stress marker malondialdehyde was increased slightly but not significantly in TES and DHEA groups. On the other hand, antioxidant enzymes such as SOD and glutathione peroxidase (GSH-Px) levels were slightly but not significantly increased in TES and DHEA groups. These data demonstrate that the potential risk to cardiac health due to exogenous androgen use may be related to oxidative stress in rats.

scholarly journals Beneficial effects of combined therapy with lacidipine and candesartan in obese hypertensive patients

2018 ◽  
Vol 56 (4) ◽  
pp. 257-264
Author(s):  
Tatiana Ashcheulova ◽  
Nina Gerasimchuk ◽  
Olga Kovalyova ◽  
Oleksii Honchar
Keyword(s):  
Oxidative Stress ◽  
Endothelial Function ◽  
Antihypertensive Therapy ◽  
Inflammatory Cytokines ◽  
Overweight And Obesity ◽  
Oxidative Stress Marker ◽  
Hypertensive Patients ◽  
Tnf Α ◽  
And Oxidative Stress ◽  
Pro Inflammatory Cytokines

Abstract Introduction. Obesity is becoming one of the leading risk factors of coronary heart disease, hypertension, cerebrovascular disease. Despite the presence of a large number of antihypertensive agents and scientific substantiation of antihypertensive treatment principles it would be wrong to assume that the problem is completely solved. Development of endothelial dysfunction is one of the key pathogenic mechanisms in hypertension. This process is proven to have contributed by immune inflammation activation which is mediated by pro-inflammatory cytokines and oxidative stress. Aims. To investigate the additional benefits of the combined antihypertensive therapy with lacidipine and candesartan on the basis of studying their antioxidant properties, impact on endothelial function and pro-inflammatory cytokines activity in hypertensive patients with overweight and obesity. Methods. A combination of a calcium channel blocker and angiotensin receptor blocker (lacidipine 2 mg, 4 mg, and candesartan 4mg, 8mg, 16mg) was prescribed to 30 patients with essential hypertension of grades 1-3, 30 to 65 years old (mean age - 54.7 ± 5.8 years), who previously have not been receiving regular antihypertensive therapy. Results. During the course of combined antihypertensive therapy with lacidipine and candesartan, a significant reduction in i-NOS activity, TNF-α to its type I soluble receptor ratio (TNF- α/sTNF-αRI), and oxidative stress marker - 8-iso-PgF2α has been observed. Activity of e-NOS, levels of SOD and catalase, in contrast, have increased by the end of observation period. Conclusion. The improvement of endothelial function due to lower level of oxidative stress and a significant decrease of immune activation has been observed in hypertensive patients with overweight and obesity under the influence of combined antihypertensive therapy with lacidipine and candesartan.

scholarly journals Tumoricidal Effect of Trigonella foenum-graceum Extract and Selenium Nanoparticles on Ehrlich Carcinoma Bearing Mice

2019 ◽  
pp. 1-16 ◽  
Author(s):  
Ahmed I. El-Batal ◽  
Neamat H. Ahmed ◽  
Lamiaa A. A. Barakat ◽  
Salma M. Khirallah
Keyword(s):  
Oxidative Stress ◽  
Tumor Size ◽  
Antitumor Effect ◽  
Caspase 3 ◽  
Granzyme B ◽  
Selenium Nanoparticles ◽  
Oxidative Stress Marker ◽  
Ehrlich Carcinoma ◽  
Tnf Α ◽  
Ifn Γ

Trigonella foenum-graceum extract either alone or combined with selenium nanoparticles exhibited antitumor effect. Ehrlich ascite carcinoma (EAC) cell line and four groups of female mice were used. Solid Ehrlich carcinoma (EC) was induced by inoculation of 2.5x106 cells in left thighs of each animal. Mice were gavage orally by 2.5 µg/0.1 ml of Trigonella foenum-graceum extract either alone or combined with selenium nanoparticles daily during one month. Tumor size, serum tumor markers (TNF-α, IFN- γ, Granzyme-B and Caspase-3) were measured. Oxidative stress, antioxidant markers, Histopathological, apoptotic and necrotic examinations were determined in tumor tissues. Tumor size of experimental groups represents reduction. Caspase-3 as well as Granzyme-B activities were significantly elevated along with diminishing tumor size while, TNF-α and IFN-γ levels were decreased in serum. Meanwhile, oxidative stress marker (MDA) was significantly decreased in tumor tissue. The tumor GSH content and CAT activity were increased. Histopathological, apoptotic and necrotic examinations were context with previous conclusion. It could be concluded that Trigonella foenum-graceum extract either alone or combined with SeNPs exhibited antitumor effect which is reflected by a inhibition in tumor size, a decrease of serum TNF-α and IFN-γ, an increase in serum caspase-3 and Granzyme-B, reduction in tumor MDA and an increase in tumor GSH and CAT which cause regulate tumor regression.

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