scholarly journals Autocrine S100B in Astrocytes Promotes VEGF-dependent Inflammation and Oxidative Stress, and Causes Impairment of Neuroprotection

2021 ◽  
Author(s):  
xuebao wang ◽  
he yu ◽  
leping liu ◽  
baihui chen ◽  
shuya feng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Encephalopathy ◽  
Inflammatory Response ◽  
Underlying Mechanism ◽  
Minimal Hepatic Encephalopathy ◽  
Comprehensive Understanding ◽  
Vegf Expression ◽  
Cox 2 ◽  
The Impact ◽  
And Oxidative Stress

Abstract Background: Our previous study revealed that minimal hepatic encephalopathy (MHE) is strongly associated with neuroinflammation. Nevertheless, the underlying mechanism of the induction of inflammatory response in MHE astrocytes remains unclear. Methods: In this study, we further investigated the effect and mechanism of S100B, predominant isoform expressed and released from mature astrocytes, on MHE-like neuropathology in the MHE rat model. Results: We discovered that S100B expressions and autocrine were significantly increased in MHE rats and astrocytes isolated from MHE rats. Furthermore, we found that S100B stimulates VEGF expression via the interaction between TLR2 and RAGE in an autocrine manner. S100B-facilitated VEGF autocrine expression further led to a VEGFR2 and COX-2 interaction, which in turn induced the activation of NFƙB, eventually resulting in inflammation and oxidative stress caused by MHE astrocytes. Compared to WT astrocytes, impairment of MHE astrocytes supported neuronal growth in co-culture.Conclusions: To sum up, comprehensive-understanding of the impact of S100B-overexpressed MHE astrocyte on MHE pathology may provide insights into the etiology of MHE.

scholarly journals Autocrine S100B in astrocytes promotes VEGF-dependent inflammation and oxidative stress, and causes impairment of neuroprotection

2021 ◽  
Author(s):  
xuebao wang ◽  
he yu ◽  
leping liu ◽  
baihui chen ◽  
shuya feng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Encephalopathy ◽  
Inflammatory Response ◽  
Underlying Mechanism ◽  
Minimal Hepatic Encephalopathy ◽  
Comprehensive Understanding ◽  
Vegf Expression ◽  
Cox 2 ◽  
The Impact ◽  
And Oxidative Stress

Abstract Minimal hepatic encephalopathy (MHE) is strongly associated with neuroinflammation. Nevertheless, the underlying mechanism of the induction of inflammatory response in MHE astrocytes remains unclear. In this study, we further investigated the effect and mechanism of S100B, predominant isoform expressed and released from mature astrocytes, on MHE-like neuropathology in the MHE rat model. We discovered that S100B expressions and autocrine were significantly increased in MHE rats and astrocytes isolated from MHE rats. Furthermore, we found that S100B stimulates VEGF expression via the interaction between TLR2 and RAGE in an autocrine manner. S100B-facilitated VEGF autocrine expression further led to a VEGFR2 and COX-2 interaction, which in turn induced the activation of NFƙB, eventually resulting in inflammation and oxidative stress caused by MHE astrocytes. Compared to WT astrocytes, impairment of MHE astrocytes supported neuronal growth in co-culture. To sum up, comprehensive-understanding of the impact of S100B-overexpressed MHE astrocyte on MHE pathology may provide insights into the etiology of MHE.

The impact of different biocompatible coated cardiopulmonary bypass circuits on inflammatory response and oxidative stress

Perfusion ◽  
2010 ◽  
Vol 25 (6) ◽  
pp. 427-429 ◽  
Author(s):  
N. Sohn ◽  
J. Marcoux ◽  
T. Mycyk ◽  
J. Krahn ◽  
QH Meng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiopulmonary Bypass ◽  
Inflammatory Response ◽  
The Impact ◽  
And Oxidative Stress

Involvement of Rho-kinase/IκB-α/NF-κB activation in IL-1β-induced inflammatory response and oxidative stress in human chondrocytes

2021 ◽  
pp. 1-9
Author(s):  
Rukiye Nalan Tiftik ◽  
Meryem Temiz-Reşitoğlu ◽  
Demet Sinem Güden ◽  
Gülsen Bayrak ◽  
İsmail Ün ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Nadph Oxidase ◽  
Rho Kinase ◽  
Human Chondrocytes ◽  
Rock Inhibitor ◽  
Pathway Activation ◽  
Tnf Α ◽  
Cox 2 ◽  
And Oxidative Stress

It has been clearly indicated that osteoarthritis (OA) is an inflammatory and degenerative disease that could be promoted by Rho-kinase (ROCK); however, little is known about the role of ROCK/inhibitor κB alpha (IκB-α)/nuclear factor-κB (NF-κB) p65 pathway activation in interleukin-1β (IL-1β) induced inflammatory response and oxidative stress in primary human chondrocytes. To test this hypothesis, we focused on determining ROCK-II, IκB-α, p-IκB-α, NF-κB p65, p-NF-κB p65, IL-6, tumor necrosis factor alpha (TNF-α), cyclooxygenase-2 (COX-2), p22phox, and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subtype 4 (NOX4) protein expression, ROCK-II activity, NADPH oxidase levels, and total antioxidant capacity (TAC) in the presence and absence of ROCK-inhibitor fasudil. IL-1β (2 ng·mL–1, 24 h) increased the expression of ROCK-II, p-IκB-α, NF-κB p65, p-NF-κB p65, IL-6, TNF-α, COX-2, and p22phox proteins, and decreased the expression of IκB-α, and the NOX4 protein level did not alter. ROCK activity and NADPH oxidase levels were increased, whereas the TAC was decreased by IL-1β. Fasudil (10−5–10−7 M) reversed all these changes induced by IL-1β. These results demonstrate that ROCK/IκB-α/NF-κB p65 pathway activation contributes to the IL-1β-induced inflammatory response and oxidative stress, and thus, ROCK inhibition might be a beneficial treatment option for OA patients mainly based on its anti-inflammatory and antioxidant effects.

The impact of different biocompatible coated cardiopulmonary bypass circuits on inflammatory response and oxidative stress

Perfusion ◽  
2009 ◽  
Vol 24 (4) ◽  
pp. 231-237 ◽  
Author(s):  
N. Sohn ◽  
J. Marcoux ◽  
T. Mycyk ◽  
J. Krahn ◽  
QH Meng
Keyword(s):  
Oxidative Stress ◽  
Cardiopulmonary Bypass ◽  
Inflammatory Response ◽  
Inflammatory Responses ◽  
Artery Bypass ◽  
Serum Levels ◽  
Control Group ◽  
Significant Difference ◽  
The Impact ◽  
And Oxidative Stress

This study was to compare the impact of different biocompatible coated circuits on inflammatory response and oxidative stress induced during cardiopulmonary bypass (CPB). Seventy-eight patients undergoing elective coronary artery bypass grafting (CABG) with CPB were randomly assigned to five groups with different biocompatible coated circuits: Trillium, Bioline, Phosphorylcholine, Polymethoxyethyl acrylate (PMEA), and the uncoated control group. Blood was drawn at three different time points: before CPB, 6 and 72 hours post CPB. Unlike the Trillium group, serum levels of TNF-α in the Bioline and Phosphorylcholine groups significantly increased only at 72 hours post CPB (p < 0.05). Serum levels of IL-6 significantly increased at 6 and 72 hours post CPB in all groups (p < 0.01). The Trillium group showed a significant increase of IL-10 compared to the control group at 72 hours post CPB (p < 0.05). Serum levels of NOx in the Phosphorylcholine group significantly decreased at 6 hours post CPB compared to baseline (p < 0.05). Both the Bioline and Phosphorylcholine groups showed statistical decreases in serum NOx levels compared with other groups at 6 hours post CPB (p < 0.05). A significant difference in NOx levels between the Bioline and the control group was also observed at 72 hours post CPB. Myeloperoxidase levels were significantly elevated at 6 and 72 hours post CPB in all groups (p < 0.05). Inflammatory response and oxidative stress are elevated during CABG with CPB. Heparin-coated and the Phosphorylcholine-coated circuits induce less inflammatory responses and oxidative stress compared to other circuits.

scholarly journals Galangin Resolves Cardiometabolic Disorders through Modulation of AdipoR1, COX-2, and NF-κB Expression in Rats Fed a High-Fat Diet

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 769
Author(s):  
Patoomporn Prasatthong ◽  
Sariya Meephat ◽  
Siwayu Rattanakanokchai ◽  
Juthamas Khamseekaew ◽  
Sarawoot Bunbupha ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Tissue ◽  
Sprague Dawley ◽  
High Fat ◽  
Impaired Liver Function ◽  
Impaired Liver ◽  
Cardiometabolic Disorders ◽  
Cox 2 ◽  
Factor Α ◽  
And Oxidative Stress

Galangin is a natural flavonoid. In this study, we evaluated whether galangin could alleviate signs of metabolic syndrome (MS) and cardiac abnormalities in rats receiving a high-fat (HF) diet. Male Sprague–Dawley rats were given an HF diet plus 15% fructose for four months, and they were fed with galangin (25 or 50 mg/kg), metformin (100 mg/kg), or a vehicle for the last four weeks. The MS rats exhibited signs of MS, hypertrophy of adipocytes, impaired liver function, and cardiac dysfunction and remodeling. These abnormalities were alleviated by galangin (p < 0.05). Interleukin-6 and tumor necrosis factor-α concentrations and expression were high in the plasma and cardiac tissue in the MS rats, and these markers were suppressed by galangin (p < 0.05). These treatments also alleviated the low levels of adiponectin and oxidative stress induced by an HF diet in rats. The downregulation of adiponectin receptor 1 (AdipoR1) and cyclooxygenase-2 (COX-2) and the upregulation of nuclear factor kappa B (NF-κB) expression were recovered in the galangin-treated groups. Metformin produced similar effects to galangin. In conclusion, galangin reduced cardiometabolic disorders in MS rats. These effects might be linked to the suppression of inflammation and oxidative stress and the restoration of AdipoR1, COX-2, and NF-κB expression.

scholarly journals Targeting ROS/NF-κB sigaling pathway by the seedless black Vitis vinifera polyphenols in CCl4-intoxicated kidney, lung, brain, and spleen in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Noha H. Habashy ◽  
Ahmad S. Kodous ◽  
Marwa M. Abu-Serie
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Vitis Vinifera ◽  
Rat Kidney ◽  
Environmental Pollutant ◽  
Enhancing Effect ◽  
Tnf Α ◽  
Cox 2 ◽  
Histopathological Studies ◽  
And Oxidative Stress

AbstractCarbon tetrachloride (CCl4) is an abundant environmental pollutant that can generate free radicals and induce oxidative stress in different human and animal organs like the kidney, lung, brain, and spleen, causing toxicity. The present study evaluated the alleviative mechanism of the isolated polyphenolic fraction from seedless (pulp and skin) black Vitis vinifera (VVPF) on systemic oxidative and necroinflammatory stress in CCl4-intoxicated rats. Here, we found that the administration of VVPF to CCl4-intoxicated rats for ten days was obviously ameliorated the CCl4-induced systemic elevation in ROS, NO and TBARS levels, as well as MPO activity. Also, it upregulated the cellular activities of the enzymatic (SOD, and GPx) and non-enzymatic (TAC and GSH) antioxidants. Furthermore, the gene expression of the ROS-related necroinflammatory mediators (NF-κB, iNOS, COX-2, and TNF-α) in the kidney, brain, and spleen, as well as IL-1β, and IL-8 in the lung were greatly restored. The histopathological studies confirmed these biochemical results and showed a noticeable enhancing effect in the architecture of the studied organs after VVPF intake. Thus, this study indicated that VVPF had an alleviative effect on CCl4-induced necroinflammation and oxidative stress in rat kidney, lung, brain, and spleen via controlling the ROS/NF-κB pathway.

Mercury Exposure and Endothelial Dysfunction

2015 ◽  
Vol 34 (4) ◽  
pp. 300-307 ◽  
Author(s):  
Swati Omanwar ◽  
M. Fahim
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Vascular Endothelium ◽  
Circulatory System ◽  
Vital Role ◽  
Mercury Exposure ◽  
And Function ◽  
The Impact ◽  
And Oxidative Stress

Vascular endothelium plays a vital role in the organization and function of the blood vessel and maintains homeostasis of the circulatory system and normal arterial function. Functional disruption of the endothelium is recognized as the beginning event that triggers the development of consequent cardiovascular disease (CVD) including atherosclerosis and coronary heart disease. There is a growing data associating mercury exposure with endothelial dysfunction and higher risk of CVD. This review explores and evaluates the impact of mercury exposure on CVD and endothelial function, highlighting the interplay of nitric oxide and oxidative stress.

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