scholarly journals Action of chondroitin sulfate on the level of cytokines and reactive oxygen species in blood serum upon carrageenan-induced inflammation

2017 ◽  
Vol 22 (1) ◽  
pp. 9-11
Author(s):  
K. Dvorshchenko ◽  
M. Ashpin ◽  
O. Korotkyi ◽  
Ye. Torgalo ◽  
T. Falalyeyeva
Keyword(s):  
Reactive Oxygen Species ◽  
Blood Serum ◽  
Chondroitin Sulfate ◽  
Inflammatory Cytokines ◽  
Superoxide Radical ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tnf Α ◽  
Rat Paw ◽  
Pro Inflammatory Cytokines

Increase of concentration of pro-inflammatory cytokines (IL-1β, TNF-α) is fixed in blood serum at carrageenan-induced rat paw inflammation, as well as increase of the content of reactive oxygen species (superoxide radical, hydrogen peroxide). At introduction of the preparation on the basis of chondroitin sulfate the level of pro-inflammatory cytokines and reactive oxygen species in blood serum decreases, while the concentration of IL10 increases in 1,7 times concerning the group of animals with сarrageenan-induced inflammation.

scholarly journals Pro-inflammatory cytokines increase reactive oxygen species through mitochondria and NADPH oxidase in cultured RPE cells

2007 ◽  
Vol 85 (4) ◽  
pp. 462-472 ◽  
Author(s):  
Dongli Yang ◽  
Susan G. Elner ◽  
Zong-Mei Bian ◽  
Gerd O. Till ◽  
Howard R. Petty ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Inflammatory Cytokines ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Rpe Cells ◽  
Pro Inflammatory Cytokines

scholarly journals Human Huntington’s disease pluripotent stem cell-derived microglia develop normally but are abnormally hyper-reactive and release elevated levels of reactive oxygen species

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Grace C. O’Regan ◽  
Sahar H. Farag ◽  
Caroline S. Casey ◽  
Alison Wood-Kaczmar ◽  
Jennifer M. Pocock ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Inflammatory Cytokines ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Protein Markers ◽  
Striatal Neurons ◽  
Human Microglia ◽  
Pro Inflammatory Cytokines

Abstract Background Neuroinflammation may contribute to the pathogenesis of Huntington’s disease, given evidence of activated microglia and elevated levels of inflammatory molecules in disease gene carriers, even those many years from symptom onset. We have shown previously that monocytes from Huntington’s disease patients are hyper-reactive to stimulation in a manner dependent on their autonomous expression of the disease-causing mutant HTT protein. To date, however, whether human microglia are similarly hyper-responsive in a cell-autonomous manner has not been determined. Methods Microglial-like cells were derived from human pluripotent stem cells (PSCs) expressing mutant HTT containing varying polyglutamine lengths. These included lines that are otherwise isogenic, such that any observed differences can be attributed with certainty to the disease mutation itself. Analyses by quantitative PCR and immunofluorescence microscopy respectively of key genes and protein markers were undertaken to determine whether Huntington’s disease PSCs differentiated normally to a microglial fate. The resultant cultures and their supernatants were then assessed by various biochemical assays and multiplex ELISAs for viability and responses to stimulation, including the release of pro-inflammatory cytokines and reactive oxygen species. Conditioned media were applied to PSC-derived striatal neurons, and vice versa, to determine the effects that the secretomes of each cell type might have on the other. Results Human PSCs generated microglia successfully irrespective of the expression of mutant HTT. These cells, however, were hyper-reactive to stimulation in the production of pro-inflammatory cytokines such as IL-6 and TNFα. They also released elevated levels of reactive oxygen species that have neurotoxic potential. Accompanying such phenotypes, human Huntington’s disease PSC-derived microglia showed increased levels of apoptosis and were more susceptible to exogenous stress. Such stress appeared to be induced by supernatants from human PSC-derived striatal neurons expressing mutant HTT with a long polyglutamine tract. Conclusions These studies show, for the first time, that human Huntington’s disease PSC-derived microglia are hyper-reactive due to their autonomous expression of mutant HTT. This provides a cellular basis for the contribution that neuroinflammation might make to Huntington’s disease pathogenesis.

scholarly journals Linagliptin Protects against Endotoxin-Induced Acute Kidney Injury in Rats by Decreasing Inflammatory Cytokines and Reactive Oxygen Species

2021 ◽  
Vol 22 (20) ◽  
pp. 11190
Author(s):  
Tsung-Jui Wu ◽  
Yi-Jen Hsieh ◽  
Chia-Wen Lu ◽  
Chung-Jen Lee ◽  
Bang-Gee Hsu
Keyword(s):  
Reactive Oxygen Species ◽  
Acute Kidney Injury ◽  
Inflammatory Cytokines ◽  
Kidney Injury ◽  
Endotoxin Shock ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Ampk Pathway ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Septic shock can increase pro-inflammatory cytokines, reactive oxygen species (ROS), and multiple organ dysfunction syndrome (MODs) and even lead to death. Dipeptidyl peptidase-4 (DPP-4) inhibitors have been proven to exert potential antioxidant and anti-inflammatory effects. We investigated the effects of linagliptin on endotoxic shock and acute kidney injury (AKI) in animal and cell models. In the cell model, linagliptin attenuated ROS by activating the AMP-activated protein kinase (AMPK) pathway, restoring nuclear-factor-erythroid-2-related factor (Nrf2) and heme oxygenase 1 (HO-1) protein, and decreasing pro-inflammatory cytokines (tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β)). In the animal model, 14-week-old conscious Wistar–Kyoto rats were randomly divided into three groups (n = 8 in each group). Endotoxin shock with MODs was induced by the intravenous injection of Klebsiella pneumoniae lipopolysaccharide (LPS, 20 mg/kg). Linagliptin improved animal survival without affecting hemodynamic profiles. In the histopathology and immunohistochemistry examinations of the rat kidneys, linagliptin (10 mg/kg) suppressed nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and inducible nitric oxide synthase (iNOS), decreased injury scores, and preserved E-cadherin expression from LPS damage. In conclusion, linagliptin ameliorated endotoxin-shock-induced AKI by reducing ROS via AMPK pathway activation and suppressing the release of TNF-α and IL-1β in conscious rats.

Camel whey protein protects lymphocytes from apoptosis via the PI3K–AKT, NF-κB, ATF-3, and HSP-70 signaling pathways in heat-stressed male mice

2018 ◽  
Vol 96 (4) ◽  
pp. 407-416 ◽  
Author(s):  
Gamal Badr ◽  
Nancy K. Ramadan ◽  
Hanem S. Abdel-Tawab ◽  
Samia F. Ahmed ◽  
Mohamed H. Mahmoud
Keyword(s):  
Reactive Oxygen Species ◽  
B Cells ◽  
Whey Protein ◽  
Inflammatory Cytokines ◽  
Reactive Oxygen ◽  
Immune Dysfunction ◽  
Oxygen Species ◽  
Male Mice ◽  
The Impact ◽  
Pro Inflammatory Cytokines

Heat stress (HS) is an environmental factor that depresses the immune systems that mediate dysfunctional immune cells. Camel whey protein (CWP) can scavenge free radicals and enhance immunity. This study investigated the impact of dietary supplementation with CWP on immune dysfunction induced by exposure to HS. Male mice (n = 45) were distributed among 3 groups: control group; HS group; and HS mice that were orally administered CWP (HS + CWP group). The HS group exhibited elevated levels of reactive oxygen species (ROS) and pro-inflammatory cytokines (interleukin (IL)-1β, IL-6, tumor necrosis factor-α) as well as a significant reduction in the IL-2 and IL-4 levels. Exposure to HS resulted in impaired phosphorylation of AKT and IκB-α (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha); increased expression of activating transcription factor 3 (ATF-3) and 70 kDa heat shock proteins (HSP70); and aberrant distribution of CD3+ T cells and CD20+ B cells in the thymus and spleen. Interestingly, HS mice treated with CWP presented significantly restored levels of reactive oxygen species and pro-inflammatory cytokines near the levels observed in the control mice. Furthermore, supplementation of HS mice with CWP enhanced the phosphorylation of AKT and IκB-α; attenuated the expression of ATF-3, HSP70, and HSP90; and improved T and B cell distributions in the thymus and spleen. Our findings reveal a potential immunomodulatory effect of CWP in attenuating immune dysfunction induced by exposure to thermal stress.

Altered composition of high-lipid diet may generate reactive oxygen species by disturbing the balance of antioxidant and free radicals

2020 ◽  
Vol 31 (3) ◽  
Author(s):  
Arnab Banerjee ◽  
Debasmita Das ◽  
Rajarshi Paul ◽  
Sandipan Roy ◽  
Ankita Bhattacharjee ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Reactive Oxygen ◽  
Control Group ◽  
Preliminary Evaluation ◽  
Oxygen Species ◽  
High Lipid ◽  
Tnf Α ◽  
High Lipid Diet ◽  
Lipid Diet

AbstractBackgroundIn the present era, obesity is increasing rapidly, and high dietary intake of lipid could be a noteworthy risk factor for the occasion of obesity, as well as nonalcoholic fatty liver disease, which is the independent risk factor for type 2 diabetes and cardiovascular disease. For a long time, high-lipid diet (HLD) in “fast food” is turning into part of our everyday life. So, we were interested in fulfilling the paucity of studies by means of preliminary evaluation of these three alternative doses of HLD on a rat model and elucidating the possible mechanism of these effects and divulging the most alarming dose.MethodsThirty-two rats were taken, and of these, 24 were fed with HLD in three distinctive compositions of edible coconut oil and vanaspati ghee in a ratio of 2:3, 3:2 and 1:1 (n = 8), orally through gavage at a dose of 10 mL/kg body weight for a period of 28 days, whereas the other eight were selected to comprise the control group.ResultsAfter completion of the experiment, followed by analysis of data it was revealed that hyperlipidemia with increased liver and cardiac marker enzymes, are associated with hepatocellular injury and cardiac damage. The data also supported increased proinflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α). As oxidative stress parameter increased in both liver and heart, there is also an increased in TNF-α due to an increased expression of inducible nitric oxide (NO) synthase, which led to a high production of NO. Moreover, HLD treatment explicitly weakens reasonability of hepatocytes and cardiomyocytes conceivably through G0/G1 or S stage capture or perhaps by means of enlistment of sub-G0/G1 DNA fragmentation and a sign of apoptosis.ConclusionsBased on the outcomes, it tends to be inferred that consequences of the present examination uncovered HLD in combination of 2:3 applies most encouraging systemic damage by reactive oxygen species generation and hyperlipidemia and necroapoptosis of the liver and heart. Hence, outcome of this study may help to formulate health care strategy and warns about the food habit in universal population regarding the use of hydrogenated and saturated fats (vanaspati ghee) in diet.

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