Reduction in TNF alpha and oxidative stress by liraglutide: Impact on ketamine-induced cognitive dysfunction and hyperlocomotion in rats

Life Sciences ◽  
2021 ◽  
pp. 119523
Author(s):  
Amina Ahmed Sedky ◽  
Yosra Magdy
Keyword(s):  
Oxidative Stress ◽  
Cognitive Dysfunction ◽  
Tnf Alpha ◽  
And Oxidative Stress

scholarly journals Antia, a Natural Antioxidant Product, Attenuates Cognitive Dysfunction in Streptozotocin-Induced Mouse Model of Sporadic Alzheimer’s Disease by Targeting the Amyloidogenic, Inflammatory, Autophagy, and Oxidative Stress Pathways

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Nesrine S. El Sayed ◽  
Mamdooh H. Ghoneum
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Diseases ◽  
Protective Effect ◽  
Cognitive Dysfunction ◽  
Protective Role ◽  
Sporadic Alzheimer’S Disease ◽  
Stat3 Pathway ◽  
And Oxidative Stress

Background. Many neurodegenerative diseases such as Alzheimer’s disease are associated with oxidative stress. Therefore, antioxidant therapy has been suggested for the prevention and treatment of neurodegenerative diseases. Objective. We investigated the ability of the antioxidant Antia to exert a protective effect against sporadic Alzheimer’s disease (SAD) induced in mice. Antia is a natural product that is extracted from the edible yamabushitake mushroom, the gotsukora and kothala himbutu plants, diosgenin (an extract from wild yam tubers), and amla (Indian gooseberry) after treatment with MRN-100. Methods. Single intracerebroventricular (ICV) injection of streptozotocin (STZ) (3 mg/kg) was used for induction of SAD in mice. Antia was injected intraperitoneally (i.p.) in 3 doses (25, 50, and 100 mg/kg/day) for 21 days. Neurobehavioral tests were conducted within 24 h after the last day of injection. Afterwards, mice were sacrificed and their hippocampi were rapidly excised, weighed, and homogenized to be used for measuring biochemical parameters. Results. Treatment with Antia significantly improved mice performance in the Morris water maze. In addition, biochemical analysis showed that Antia exerted a protective effect for several compounds, including GSH, MDA, NF-κB, IL-6, TNF-α, and amyloid β. Further studies with western blot showed the protective effect of Antia for the JAK2/STAT3 pathway. Conclusions. Antia exerts a significant protection against cognitive dysfunction induced by ICV-STZ injection. This effect is achieved through targeting of the amyloidogenic, inflammatory, and oxidative stress pathways. The JAK2/STAT3 pathway plays a protective role for neuroinflammatory and neurodegenerative diseases such as SAD.

scholarly journals Neuroprotective effects of Withania somnifera in BPA induced-cognitive dysfunction and oxidative stress in mice

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Hareram Birla ◽  
Chetan Keswani ◽  
Sachchida Nand Rai ◽  
Saumitra Sen Singh ◽  
Walia Zahra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Dysfunction ◽  
Withania Somnifera ◽  
Neuroprotective Effects ◽  
And Oxidative Stress

Inhibition of Cancer and Drug-Associated Thrombosis Using Novel Inhibitors of NF-κB and Oxidative Stress Pathways.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3937-3937
Author(s):  
Shaker A. Mousa ◽  
Ahmad Aljada ◽  
Shyam Patil ◽  
Shymaa S. Mousa
Keyword(s):  
Oxidative Stress ◽  
Human Plasma ◽  
Tissue Factor ◽  
Human Blood ◽  
Fibrin Clot ◽  
Chemotherapeutic Agents ◽  
Tnf Alpha ◽  
Down Regulation ◽  
Cancer Types ◽  
And Oxidative Stress

Abstract Background: Venous thromboemblism is associated with a systemic hypercoagulable state that is secondary to tumor or proinflammatory activation of procoagulant mechanisms, as well as down-regulation of anticoagulant mechanisms. In the present investigation, the potential antithrombotic efficacy and mechanism for OT-304 analogs, novel small molecules targeting NFkB and oxidative stress pathways, was examined in various cellular systems. Methods: Human monocytic cells were incubated with OT-304 analogs for 3 hours and then stimulated with LPS (25 ng/ml) for another 3 hours. Real-time PCR for NF-κB (P50/P65 complex) nuclear translocation dynamics, TNF-alpha, EGR1, and tissue factor (TF) was then performed. Additionally, the effect of OT-304 analogs on oxidative stress, inflammation, and procoagulant pathways in human monocytes and endothelial cells were performed using Affymatrix Microarray. Furthermore, the anticoagulant efficacy of OT-304 analogs as compared to classical anticoagulants such as Low Molecular weight Heparins (LMWH) was determined in proinflammatory-mediated hypercoagulable state, cancer, and/or chemotherapy-associated platelet/fibrin clot formation assays using thrombelastography (TEG). TEG was performed using blood from healthy volunteers. Clot dynamics were initiated using different activators of coagulation that included different cancer types, different chemotherapeutic agents, and standard anti-angiogenesis agents such as bevacizumab, ranibizumab and others in human blood. Additionally, effects of OT-304 analogs as compared to unfractionated heparin and the LMWH enoxaparin on activated partial thromboplastin time (aPTT) in human plasma was carried out using a fibrometric method. Results: OT-304 analogs effectively inhibited NF-κB and oxidative stress pathways leading to down-regulation of cytokines and chemokines, including TNF-alpha. OT-304 analogs effectively inhibited EGR1, which was associated with down-regulation of the key procoagulant mediator tissue factor (TF). In human blood, OT-304 effectively inhibited hypercoagulation and prothrombotic states mediated by proinflammatory stimuli including LPS, NF-κB activators such as ceramide, different cancer types such as pancreatic, glioma and lung cancer, different chemotherapeutic agents such as doxorubicin and etopocide, and angiogenesis inhibitors such as bevacizumab (Avastin) or ranibizumab (Lucentis) as evident from the inhibition of platelet-fibrin clot dynamics. The IC50 required for blocking cancer or drug-associated thrombosis ranged from 1–3 uM. OT-304 analogs did not have any effect on aPTT up to concentrations ranging from 1– 100 uM in human plasma. In contrast, heparin or LMWH resulted in a dose-dependent (0.001 – 1 ug/ml) increase in aPTT. These data suggest OT-304 effectively inhibits prothrombotic events, regardless of the stimulus, with potentially no effect on hemostasis. Conclusions: OT304 analogs, by virtue of their ability to target and modulate more than one pathway, may represent a promising therapeutic strategy for inhibiting thrombosis associated with inflammation, cancer, and chemotherapy plus other adjunct therapies without compromising hemostasis.

Amelioration of scopolamine induced cognitive dysfunction and oxidative stress by Inonotus obliquus– a medicinal mushroom

2011 ◽  
Vol 2 (6) ◽  
pp. 320 ◽  
Author(s):  
Vijayasree Vayalanellore Giridharan ◽  
Rajarajan Amirthalingam Thandavarayan ◽  
Tetsuya Konishi
Keyword(s):  
Oxidative Stress ◽  
Cognitive Dysfunction ◽  
Medicinal Mushroom ◽  
Inonotus Obliquus ◽  
And Oxidative Stress

Inhibition of phosphodiesterase-4 reverses the cognitive dysfunction and oxidative stress induced by Aβ25–35 in rats

2016 ◽  
Vol 31 (4) ◽  
pp. 779-791 ◽  
Author(s):  
Yeye Zhuo ◽  
Haibiao Guo ◽  
Yufang Cheng ◽  
Chuang Wang ◽  
Canmao Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Dysfunction ◽  
Phosphodiesterase 4 ◽  
And Oxidative Stress

Study on role of TNF-[alpha] and oxidative stress in pathogenesis of type 2 diabetes mellitus

2016 ◽  
Author(s):  
Talat Saatov ◽  
Zafar Ibragimov ◽  
Sanobarxon Irgasheva ◽  
Elvira Ibragimova ◽  
Bakhodir Zainutdinov ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Tnf Alpha ◽  
And Oxidative Stress

P2-023: SLEEP DEPRIVATION INDUCES COGNITIVE DYSFUNCTION THROUGH MECHANISM INVOLVED IN NEUROINFLAMMATION AND OXIDATIVE STRESS

2014 ◽  
Vol 10 ◽  
pp. P478-P478
Author(s):  
Kyoung Ja Kwon ◽  
Seol-Heui Han ◽  
Ileok Jung ◽  
Chan Young Shin ◽  
Eun Joo Lee
Keyword(s):  
Oxidative Stress ◽  
Sleep Deprivation ◽  
Cognitive Dysfunction ◽  
And Oxidative Stress

scholarly journals Electroacupuncture reduces astrocyte number and oxidative stress in aged rats with surgery-induced cognitive dysfunction

2019 ◽  
Vol 47 (8) ◽  
pp. 3860-3873 ◽  
Author(s):  
Pei-Rong Liu ◽  
Feng Cao ◽  
Yu Zhang ◽  
Sheng Peng
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Cognitive Dysfunction ◽  
Neurotrophic Factor ◽  
Calcium Binding ◽  
Postoperative Cognitive Dysfunction ◽  
Neuron Specific Enolase ◽  
Left Lobe ◽  
Sprague Dawley ◽  
And Oxidative Stress

Objectives To investigate the effects of electroacupuncture in regulating astrocytes and oxidative stress in a rat model of postoperative cognitive dysfunction (POCD). Methods Male aged Sprague-Dawley rats were randomized to undergo left hepatic lobe resection to induce POCD, followed by either electroacupuncture or no treatment; or similar surgery without left lobe resection or electroacupuncture (sham). Postsurgical cognitive function, hippocampal astrocyte number and oxidative stress indicators were measured. Results At days 1, 3 and 7 following surgery, escape latency was significantly shorter and platform crossing frequency was increased with electroacupuncture versus other groups. At postoperative day 1, the electroacupuncture group showed significantly fewer glial fibrillary acidic protein (GFAP)-positive hippocampal astrocytes versus the POCD model group. In POCD rats, electroacupuncture significantly decreased serum S100 calcium binding protein B and neuron-specific enolase levels, and increased brain-derived neurotrophic factor and glial cell-derived neurotrophic factor levels, at days 1, 3 and 7. Electroacupuncture significantly attenuated the hippocampal POCD-induced increase in malondialdehyde and decreased superoxide dismutase levels at day 1 following surgery. Conclusion Electroacupuncture may improve cognitive function in rats with POCD by reducing hippocampal GFAP-positive astrocyte number and suppressing oxidative stress.

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