Protection of Human Fibroblasts from Reactive Oxygen Species by Green Tea Polyphenolic Compounds

2005 ◽  
Vol 288-289 ◽  
pp. 665-668 ◽  
Author(s):  
Dong Wook Han ◽  
H.H. Kim ◽  
Hyun Joo Son ◽  
Hyun Sook Baek ◽  
Kwon Yong Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Green Tea ◽  
Human Fibroblasts ◽  
Reactive Oxygen ◽  
High Sensitivity ◽  
Dermal Fibroblasts ◽  
Oxygen Species ◽  
A Cell ◽  
Fcm Analysis

The potential protective roles played by green tea compounds (GTPCs) against reactive oxygen species-induced oxidative stress in cultured fetal human dermal fibroblasts (fHDFs) were investigated according to cell viability measurement methods, such as fluorescence double staining followed by flow cytometry (FCM), MTT assay and crystal violet uptake. Oxidative stress was induced in the fHDFs, either by adding 50 mM H2O2 or by the action of 40 U/L xanthine oxidase (XO) in the presence of xanthine (250 µM). FCM analysis was the most suitable to show that both treatments produced a significant (p < 0.05) reduction in the fHDF viability, attributed to its high sensitivity. On the microscopic observations, the cell death with necrotic morphology was appreciably induced by both treatments. These oxidative stress-induced damages were significantly (p < 0.05) prevented by pre-incubating the fHDFs with 200 µg/ml GTPC for 1 h. These results suggest that GTPC can act as a biological antioxidant in a cell culture experimental model and prevent oxidative stress-induced cytotoxicity in cells.

scholarly journals Sildenafil Reduces Expression and Release of IL-6 and IL-8 Induced by Reactive Oxygen Species in Systemic Sclerosis Fibroblasts

2020 ◽  
Vol 21 (9) ◽  
pp. 3161 ◽  
Author(s):  
Luigi Di Luigi ◽  
Paolo Sgrò ◽  
Guglielmo Duranti ◽  
Stefania Sabatini ◽  
Daniela Caporossi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Systemic Sclerosis ◽  
Tissue Damage ◽  
Human Fibroblasts ◽  
Reactive Oxygen ◽  
Dermal Fibroblasts ◽  
Vascular Damage ◽  
Oxygen Species ◽  
Phosphodiesterase Type 5 Inhibitor

Oxidative stress linked to vascular damage plays an important role in the pathogenesis of systemic sclerosis (SSc). Indeed, vascular damage at nailfold capillaroscopy in patients with Raynaud’s Phenomenon (RP) is a major risk factor for the development of SSc together with the presence of specific autoantiobodies. Here, we investigated the effects of the phosphodiesterase type 5 inhibitor (PDE5i) sildenafil, currently used in the management of RP, in modulating the proinflammatory response of dermal fibroblasts to oxidative stress in vitro. Human fibroblasts isolated from SSc patients and healthy controls were exposed to exogenous reactive oxygen species (ROS) (100 µM H2O2), in the presence or absence of sildenafil (1 µM). Treatment with sildenafil significantly reduced dermal fibroblast gene expression and cellular release of IL-6, known to play a central role in the pathogenesis of tissue damage in SSc and IL-8, directly induced by ROS. This reduction was associated with suppression of STAT3-, ERK-, NF-κB-, and PKB/AKT-dependent pathways. Our findings support the notion that the employment of PDE5i in the management of RP may be explored for its efficacy in modulating the oxidative stress-induced proinflammatory activation of dermal fibroblasts in vivo and may ultimately aid in the prevention of tissue damage caused by SSc.

Reactive oxygen species generated by renal ischemia and reperfusion trigger protection against subsequent renal ischemia and reperfusion injury in mice

2010 ◽  
Vol 298 (1) ◽  
pp. F158-F166 ◽  
Author(s):  
Jinu Kim ◽  
Hee-Seong Jang ◽  
Kwon Moo Park
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Renal Ischemia ◽  
Ischemia And Reperfusion ◽  
Oxygen Species ◽  
Ischemia And Reperfusion Injury ◽  
A Cell ◽  
Copper Zinc ◽  
And Oxidative Stress

Ischemic preconditioning by a single event of ischemia and reperfusion (SIRPC) dramatically protects renal function against ischemia and reperfusion (I/R) induced several weeks later. We recently reported that reactive oxygen species (ROS) and oxidative stress were sustained in a kidney that had functionally recovered from I/R injury, thus suggesting an association between SIRPC and ROS and oxidative stress. However, the role of ROS in SIRPC remains to be clearly elucidated. To assess the involvement of ROS in SIRPC, mice were subjected to SIRPC (30 min of bilateral renal ischemia and 8 days of reperfusion) and then exposed to I/R injury. Thirty minutes of bilateral renal ischemia in the non-SIRPC mice resulted in a marked increase in plasma creatinine levels 4 and 24 h after reperfusion, which was not observed in the I/R in the SIRPC mice. SIRPC resulted in increases in the levels of kidney superoxide. Administrations of manganese(III) tetrakis(1-methyl-4-pyridyl) porphyrin [MnTMPyP; a cell-permeable superoxide dismutase (SOD) mimetic] and N-acetylcysteine (NAc; a ROS scavenger) to SIRPC mice blocked the SIRPC-induced increase in superoxide levels and removed ∼48–64% of the functional protection of the SIRPC kidney. Additionally, these administrations significantly inhibited I/R-induced increases in superoxide formation, hydrogen peroxide production, and lipid peroxidation, along with the inhibition of I/R-induced reductions in the expression and activity of manganese SOD, copper-zinc SOD, and catalase. Furthermore, administrations of MnTMPyP or NAc inhibited the SIRPC-induced increase in inducible nitric oxide synthase expression but did not inhibit the SIRPC-induced increases in heat shock protein-25 expression. In conclusion, the renoprotection afforded by SIRPC was triggered by ROS generated by SIRPC.

scholarly journals The Leaf Extract of Coccinia grandis (L.) Voigt Accelerated In Vitro Wound Healing by Reducing Oxidative Stress Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Poommaree Namchaiw ◽  
Yamaratee Jaisin ◽  
Cholticha Niwaspragrit ◽  
Kittiya Malaniyom ◽  
Anyamanee Auvuchanon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Wound Healing ◽  
Leaf Extract ◽  
Human Fibroblasts ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Stress Injury ◽  
Ic50 Value

The impairment in the regulation of the physiological process in the inflammatory phase of wound healing results in oxidative stress damage, which increases the severity and extends the healing time. In this study, we aimed to evaluate the radical scavenging properties of Coccinia leaf extract and its ability to ameliorate a migration process in vitro. Coccinia is a medicinal plant that was used in ancient times for relieving insect bite itching and swelling. However, the role of Coccinia leaf extract as an antioxidant related to the process of wound healing has never been studied. In this study, we demonstrated that the leaf extract possessed antioxidant properties that acted as a proton donor to neutralize reactive oxygen species with the IC50 value of 4.85 mg/mL of the extract. It could chelate iron with the IC50 value of 21.39 mg/mL of the extract. The leaf extract protected the human fibroblasts and keratinocytes from hydrogen peroxide-induced oxidative stress by increasing cell survival rate by more than 20% in all test doses. The protective property was dose-dependently correlated with the decrease in reactive oxygen species formation. In addition, the leaf extract enhanced the cell migration rate of fibroblasts and keratinocytes up to 23% compared with vehicle control. The results suggested that Coccinia leaf extract may be a potential herb for increasing the wound healing process with its antioxidant capacity and can be used as an herbal ingredient for the utilization of skincare products.

Determination of Reactive Oxygen Species in Cigarette Smoke by DR6G Fluorescent Probe

2011 ◽  
Vol 361-363 ◽  
pp. 1863-1867 ◽  
Author(s):  
Li Liu ◽  
Shi Jie Xu ◽  
Song Zhan Li
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Fluorescent Probe ◽  
Cigarette Smoke ◽  
Reactive Oxygen ◽  
High Sensitivity ◽  
Oxygen Species ◽  
Irreversible Damage ◽  
Standard Curve ◽  
Close Relationship

A mass of reactive oxygen species(ROS) are produced in the process of smoking. Superfluous ROS can induce the oxidative stress in organism, which will cause irreversible damage to cells. Fluorescent probe is taken as a marker of oxidative stress in biology and has been applied to ROS detection in the field of biology and chemistry for high sensitivity, high simplicity of data collection and high resolution. As one type of fluorescent probe, no-fluorescent dihydrorhodamine 6G(dR6G) will be oxidized to the fluorescent rhodamine 6G. In this process, each molecule reacts with two active oxygen molecules. The probe can be used to detect ROS in mainstream cigarette smoke by using derivative fluorescence method. The action mechanism of ROS on dR6G was investigated and the standard curve of R6G fluorescence intensity with its content was built up. The contents of ROS from the 4 types of cigarettes purchased in market were detected and the cleaning ability of filter tip to ROS in cigarette smoke was also researched. The result shows that the amount of ROS has close relationship with the types of tobacco and cigarette production technology and the cleaning ability of filter tip to ROS in cigarette smoke is very limited. Compared with other detecting methods such as electronic spin resonance(ESR), chromatography and mass spectrometry, this detection method by the fluorescent probe has higher efficiency and sensitivity and will have wide applications in the ROS detection fields.

scholarly journals AB0089 SILDENAFIL COUNTERACTS THE ACTIVATION OF CXCR3/CXCL10, -11 AXIS IN SCLERODERMA FIBROBLASTS EXPOSED TO REACTIVE OXYGEN SPECIES

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1074.1-1074
Author(s):  
C. Antinozzi ◽  
I. Dimauro ◽  
P. Sgrò ◽  
D. Caporossi ◽  
F. Del Galdo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Systemic Sclerosis ◽  
Reactive Oxygen ◽  
Dermal Fibroblasts ◽  
Vascular Damage ◽  
Healthy Controls ◽  
Oxygen Species ◽  
Luminex Technology

Background:Oxidative stress associated with vascular damage represents one the major contributor in the pathogenesis of systemic sclerosis (SSc) [1]. Indeed, different studies demonstrated that excessive free radicals production can contribute to the activation of fibrotic process in the skin and visceral organs [1]. CXCL10 and CXCL11, together with their receptor CXCR3, are involved in vascular damage and in fibrosis [2]. Furthermore, these chemokines have been proposed as biomarkers of vascular damage progression and severe SSc prognosis [3].Emerging evidences highlight the beneficial effects of the phosphodiesterase type 5 (PDE5) inhibitor, sildenafil, to protect different cell types from reactive oxygen species (ROS)-induced DNA damage, in vitro [3]. This effect has been linked to modulation of CXCL10 concentration in different pathological conditions [4,5].Objectives:Here we set out to investigate the effects of sildenafil, in modulating the CXCR3/CXCL10, -11 inflammatory axis in dermal fibroblasts exposed to oxidative stress, in vitro.Methods:Human dermal fibroblasts isolated by SSc skin biopsies were treated for 24h with 100µM of hydrogen peroxide (H2O2), in the presence or not of sildenafil (1µM). Dermal fibrobalsts from healthy skin were used as controls. CXCL10 and CXCL11 were evaluated in cell medium by luminex technology assay; expression of chemokine receptor (CXCR)3 and peroxisome proliferator-activated receptor (PPARγ) (a regulator of CXCL10,-11 mRNA) was evaluated by western blot assay.Results:As showed in figure 1, SSc fibroblasts (grey bar) showed similar basal levels of CXCL10 (A) and CXCL11 (B) to healthy controls (black bar). H2O2 induced a significant increase of both chemokines only in SSc fibroblasts (by 4.6 fold for CXCL10 and by 4.2 fold for CXCL11) (*P<0.05 and **P<0.01 vs. c; #P<0.05 vs. healthy controls). Sildenal pre-incubation reduced by approximatively 50% the effects of H2O2 on chemokines release (Figure 1A and B) (§P<0.05 vs. H2O2), and reduced the expression of CXCR3 and PPARγ induced by hydrogen peroxyde exposure (data not shown).Conclusion:In vitro study on dermal fibroblasts support clinical studies to determine the efficacy of sildenafil in the preventing tissue damage and fibrosis in SSc, by reducing the pro-inflammatory activation induced by oxidative stress.References:[1]Di Luigi L, Sgrò P, Duranti G, Sabatini S, Caporossi D, Del Galdo F, Dimauro I, Antinozzi C. Sildenafil Reduces Expression and Release of IL-6 and IL-8 Induced by Reactive Oxygen Species in Systemic Sclerosis Fibroblasts. Int J Mol Sci. 2020 Apr 30;21(9):3161. doi: 10.3390/ijms21093161. PMID: 32365773; PMCID: PMC7246497.[2]Koper OM, Kamińska J, Sawicki K, Kemona H. CXCL9, CXCL10, CXCL11, and their receptor (CXCR3) in neuroinflammation and neurodegeneration. Adv Clin Exp Med. 2018 Jun;27(6):849-856. doi: 10.17219/acem/68846. PMID: 29893515.[3]Crescioli C, Corinaldesi C, Riccieri V, Raparelli V, Vasile M, Del Galdo F, Valesini G, Lenzi A, Basili S, Antinozzi C. Association of circulating CXCL10 and CXCL11 with systemic sclerosis. Ann Rheum Dis. 2018 Dec;77(12):1845-1846. doi: 10.1136/annrheumdis-2018-213257. Epub 2018 May 14. PMID: 29760155; PMCID: PMC6241615.[4]Giannattasio S, Corinaldesi C, Colletti M, Di Luigi L, Antinozzi C, Filardi T, Scolletta S, Basili S, Lenzi A, Morano S, Crescioli C. The phosphodiesterase 5 inhibitor sildenafil decreases the proinflammatory chemokine IL-8 in diabetic cardiomyopathy: in vivo and in vitro evidence. J Endocrinol Invest. 2019 Jun;42(6):715-725. doi: 10.1007/s40618-018-0977-y. Epub 2018 Nov 10. PMID: 30415310; PMCID: PMC6531405.[5]You N, Li J, Huang X, Wu K, Tang Y, Wang L, Li H, Mi N, Zheng L. COMMD7 activates CXCL10 production by regulating NF-κB and the production of reactive oxygen species. Mol Med Rep. 2018 May;17(5):6784-6788. doi: 10.3892/mmr.2018.8706. Epub 2018 Mar 8. PMID: 29532873.Disclosure of Interests:None declared

scholarly journals Oxidative Stress Induced by Reactive Oxygen Species (ROS) and NADPH Oxidase 4 (NOX4) in the Pathogenesis of the Fibrotic Process in Systemic Sclerosis: A Promising Therapeutic Target

2021 ◽  
Vol 10 (20) ◽  
pp. 4791
Author(s):  
Sonsoles Piera-Velazquez ◽  
Sergio A. Jimenez
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Systemic Sclerosis ◽  
Nadph Oxidase ◽  
Therapeutic Target ◽  
Reactive Oxygen ◽  
Dermal Fibroblasts ◽  
Ros Production ◽  
Oxygen Species ◽  
Fibrotic Process

Numerous clinical and research investigations conducted during the last two decades have implicated excessive oxidative stress caused by high levels of reactive oxygen species (ROS) in the development of the severe and frequently progressive fibrotic process in Systemic Sclerosis (SSc). The role of excessive oxidative stress in SSc pathogenesis has been supported by the demonstration of increased levels of numerous biomarkers, indicative of cellular and molecular oxidative damage in serum, plasma, and other biological fluids from SSc patients, and by the demonstration of elevated production of ROS by various cell types involved in the SSc fibrotic process. However, the precise mechanisms mediating oxidative stress development in SSc and its pathogenetic effects have not been fully elucidated. The participation of the NADPH oxidase NOX4, has been suggested and experimentally supported by the demonstration that SSc dermal fibroblasts display constitutively increased NOX4 expression and that reduction or abrogation of NOX4 effects decreased ROS production and the expression of genes encoding fibrotic proteins. Furthermore, NOX4-stimulated ROS production may be involved in the development of certain endothelial and vascular abnormalities and may even participate in the generation of SSc-specific autoantibodies. Collectively, these observations suggest NOX4 as a novel therapeutic target for SSc.

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