scholarly journals Levels of Cyclooxygenase 2, Interleukin-6, and Tumour Necrosis Factor-α in Fibroblast Cell Culture Models after Photobiomodulation at 660 nm

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Asma Shaikh-Kader ◽  
Nicolette N. Houreld ◽  
Naresh K. Rajendran ◽  
Heidi Abrahamse
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
Tumour Necrosis ◽  
Fibroblast Cell ◽  
Tnf Α ◽  
Culture Models ◽  
Fibroblast Cell Culture ◽  
Cox 2 ◽  
Cell Culture Models ◽  
Necrosis Factor

Chemicals and signaling molecules released by injured cells at the beginning of wound healing prompt inflammation. In diabetes, prolonged inflammation is one of the probable causes for delayed wound healing. Increased levels of cyclooxygenase-2 (cox-2), interleukin–6 (IL-6), and tumour necrosis factor-alpha (TNF-α) are associated with the inflammatory response and in diabetes, and increased levels of these contribute to chronic wounds that do not heal. Rising levels of cox-2, IL-6, and TNF-α have also been associated with increased oxidative stress. Photobiomodulation (PBM) may impact wound healing processes by affecting the signaling pathways and molecules pertinent to tissue repair. In the present study, the effect of PBM (wavelength: 660 nm; energy density: 5 J/cm2) on levels of cox-2, IL-6, and TNF-α was determined in fibroblast cell culture models. Four WS1 models (normal, normal wounded, diabetic, and diabetic wounded) were irradiated at 660 nm, and the culture media was collected at 0, 24, and 48 h postirradiation. Cells that were not irradiated (0 J/cm2) served as the controls. The following parameters were determined postirradiation: cell morphology using light microscopy, cell viability using the Trypan Blue exclusion assay, and levels of the inflammatory markers cox-2, IL-6, and TNF-α were measured using ELISA. Cell migration increased in the wounded groups over the 48 h interval after PBM; viability improved postirradiation in the diabetic wounded groups at 0 and 24 h ( P ≤ 0.05 and P ≤ 0.01 , respectively); levels of cox-2 decreased in normal and diabetic wounded groups at 0 h ( P ≤ 0.001 ) and increased in the diabetic and diabetic wounded groups at 48 h postirradiation ( P ≤ 0.05 and P ≤ 0.01 , respectively), while levels of IL-6 decreased in the normal ( P ≤ 0.01 ), diabetic ( P ≤ 0.05 ), and diabetic wounded ( P ≤ 0.001 ) groups at 24 h and in the diabetic and diabetic wounded groups at 48 h ( P ≤ 0.05 ) postirradiation. TNF-α was decreased in the normal wounded groups ( P ≤ 0.05 ) at 48 h. Through its effect on decreased IL-6 levels in diabetic cell models, PBM at 660 nm may be successful at decreasing oxidative stress; however, the present study also found an increase in cox-2 levels at 48 h postirradiation.

scholarly journals The Influence of Interleukin (IL)-1β and IL-6 and Tumour Necrosis Factor-α on Prostaglandin Secretion from Porcine Myometrium during the First Third of Pregnancy

2010 ◽  
Vol 79 (4) ◽  
pp. 559-569 ◽  
Author(s):  
Barbara Jana ◽  
Marlena Koszykowska ◽  
Aneta Andronowska
Keyword(s):  
Protein Expression ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Uterine Contraction ◽  
Tumour Necrosis Factor Α ◽  
Cytokine Network ◽  
Tnf Α ◽  
Cox 2 ◽  
Factor Α ◽  
Necrosis Factor

The present study was undertaken to determine the effect of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) on prostaglandin (PG)F2α and PGE2 secretion as well as cyclooxygenase-2 (COX-2) protein expression in myometrium collected on days 25, 30 and 40 of pregnancy in pigs. Myometrial slices were incubated for 16 h with IL-1β, IL-6 and TNF-α (1 or 10 ng/ml of medium) or two combinations of the three cytokines (1 or 10 ng/ml of each cytokine per combination). We demonstrated the stimulatory effect of IL-1β and IL-6 on PGF2α and PGE2 secretion from myometrium collected on all examined days of pregnancy, excepting of influence of IL-6 on release of PGF2α by tissue from day 30. In turn, TNF-α was able to stimulate only PGE2 secretion by myometrium of 40-day-pregnant gilts. The three cytokines applied in combination augmented release of PGE2 from myometrium collected on days 30 and 40 of pregnancy. Stimulation of PGE2 secretion by cytokines used individually was more frequent than that of PGF2α. Moreover, an enhancement in PGF2α and/or PGE2 release was accompanied by an increase of COX-2 protein expression. Our study shows the ability of cytokines to stimulate PGF2α and PGE2 release by porcine myometrium from the first third of pregnancy. Obtained data suggest that locally PGs produced in myometrium influencing the uterine contraction activity may be important for the maintenance of myometrial quiescence during pregnancy and confirm also that the complex cytokine network is an important regulatory mechanism of PGs production during pregnancy.

Differential Effects of Corticosteroids on The Expression of Cyclooxygenase-2, Tumour Necrosis Factor-Alpha and Matrix Metalloproteinase-9 in An Animal Model of Migraine

Cephalalgia ◽  
2008 ◽  
Vol 28 (11) ◽  
pp. 1179-1187 ◽  
Author(s):  
G-M Kim ◽  
K-S Jin ◽  
C-S Chung
Keyword(s):  
Animal Model ◽  
Inflammatory Mediators ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Alpha ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Cox 2 ◽  
Metalloproteinase 9 ◽  
Necrosis Factor

Nitric oxide (NO) directly activates trigeminal afferents innervating the dura mater and up-regulates inflammatory mediators. We evaluated NO-mediated up-regulation of cyclooxygenase-2 (COX-2), tumour necrosis factor-alpha (TNF-α) and matrix metalloproteinase-9 (MMP-9), and the effect of glucocorticoid administration in an experimental animal model of migraine. COX-2 and TNF-α expression and MMP-9 activity were increased after continuous intravenous infusion of glyceryl trinitrate (GTN), a NO donor. Immunofluorescence staining demonstrated strong expression of these inflammatory mediators in the meningeal blood vessels. Methylprednisolone (MP) down-regulated MMP-9, which was reversed by RU486, a glucocorticoid receptor antagonist. COX-2 and TNF-α expression was not affected by MP or RU486 administration. These results suggest proinflammatory mediators are involved in the NO-mediated cascade of migraine pathogenesis. Further understanding of the activation of these inflammatory mediators at the transcriptional level may have therapeutic implications for future migraine treatments.

scholarly journals Terminalia catappa Extract Palliates Redox Imbalance and Inflammation in Diabetic Rats by Upregulating Nrf-2 Gene

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Franklyn Nonso Iheagwam ◽  
Gaber El-Saber Batiha ◽  
Olubanke Olujoke Ogunlana ◽  
Shalom Nwodo Chinedu
Keyword(s):  
Oxidative Stress ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Diabetic Rat ◽  
Antioxidant Enzyme Activities ◽  
Related Factor ◽  
Necrosis Factor Alpha ◽  
Terminalia Catappa ◽  
Tnf Α ◽  
Necrosis Factor

This study aims at evaluating the ameliorative role of Terminalia catappa aqueous leaf extract (TCA) on hyperglycaemia-induced oxidative stress and inflammation in a high-fat, low dose streptozotocin-induced type 2 diabetic rat model. Experimental rats were treated orally with 400 and 800 mg/kg bw TCA daily for four weeks. Antioxidant enzyme activities, plasma glucose concentration, protein concentration, oxidative stress, and inflammation biomarkers were assayed using standard methods. Hepatic relative expressions of tumour necrosis factor-alpha (TNF-α), interleukin-six (IL-6), and nuclear factor-erythroid 2 related factor 2 (Nrf-2) were also assessed. Molecular docking and prediction of major TCA phytoconstituents’ biological activity related to T2DM-induced oxidative stress were evaluated in silico. Induction of diabetes significantly ( p < 0.05 ) reduced superoxide dismutase, glutathione-S-transferase, and peroxidase activities. Glutathione and protein stores were significantly ( p < 0.05 ) depleted, while glucose, MDA, interleukin-six (IL-6), and tumour necrosis factor-α (TNF-α) concentrations were significantly ( p < 0.05 ) increased. A significant ( p < 0.05 ) upregulation of hepatic TNF-α and IL-6 expression and downregulation ( p < 0.05 ) of Nrf-2 expression were observed during diabetes onset. TCA treatment significantly ( p < 0.05 ) modulated systemic diabetic-induced oxidative stress and inflammation, mRNA expression dysregulation, and dysregulated macromolecule metabolism. However, only 800 mg/kg TCA treatment significantly ( p < 0.05 ) downregulated hepatic TNF-α expression. 9-Oxabicyclo[3.3.1]nonane-2,6-diol and 1,2,3-Benzenetriol bound comparably to glibenclamide in Nrf-2, IL-6, and TNF-α binding pockets. They were predicted to be GST A and M substrate, JAK2 expression, ribulose-phosphate 3-epimerase, NADPH peroxidase, and glucose oxidase inhibitors. These results suggest that TCA ameliorates hyperglycaemia-induced oxidative stress and inflammation by activating Nrf-2 gene.

scholarly journals Hypoxia-Induced S100A8 Expression Activates Microglial Inflammation and Promotes Neuronal Apoptosis

2021 ◽  
Vol 22 (3) ◽  
pp. 1205
Author(s):  
Ji Sun Ha ◽  
Hye-Rim Choi ◽  
In Sik Kim ◽  
Eun-A Kim ◽  
Sung-Woo Cho ◽  
...  
Keyword(s):  
Calcium Binding ◽  
Neuronal Apoptosis ◽  
Microglial Cells ◽  
Molecular Pattern ◽  
Extracellular Signal ◽  
Tnf Α ◽  
Cox 2 ◽  
Necrosis Factor ◽  
Microglial Inflammation ◽  
Tlr4 Receptor

S100 calcium-binding protein A8 (S100A8), a danger-associated molecular pattern, has emerged as an important mediator of the pro-inflammatory response. Some S100 proteins play a prominent role in neuroinflammatory disorders and increase the secretion of pro-inflammatory cytokines in microglial cells. The aim of this study was to determine whether S100A8 induced neuronal apoptosis during cerebral hypoxia and elucidate its mechanism of action. In this study, we reported that the S100A8 protein expression was increased in mouse neuronal and microglial cells when exposed to hypoxia, and induced neuroinflammation and neuronal apoptosis. S100A8, secreted from neurons under hypoxia, activated the secretion of tumor necrosis factor (TNF-α) and interleukin-6 (IL-6) through phosphorylation of extracellular-signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) in microglia. Also, phosphorylation of ERK via the TLR4 receptor induced the priming of the NLRP3 inflammasome. The changes in Cyclooxygenase-2 (COX-2) expression, a well-known inflammatory activator, were regulated by the S100A8 expression in microglial cells. Knockdown of S100A8 levels by using shRNA revealed that microglial S100A8 expression activated COX-2 expression, leading to neuronal apoptosis under hypoxia. These results suggested that S100A8 may be an important molecule for bidirectional microglia-neuron communication and a new therapeutic target for neurological disorders caused by microglial inflammation during hypoxia.

Sign in / Sign up

Export Citation Format

Share Document