Far Infrared Technology (FIT) Therapy Patches, Protects from Inflammation, Oxidative Stress and Promotes Cellular Vitality

2020 ◽  
Vol 26 (34) ◽  
pp. 4323-4329
Author(s):  
Donatella Pastore ◽  
Francesca Pacifici ◽  
Giampaolo Ciao ◽  
Valentina Bedin ◽  
Guido Pasquantonio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Molecular Mechanisms ◽  
Far Infrared ◽  
Hek 293 ◽  
Markers Of Inflammation ◽  
Therapeutic Benefits ◽  
Tnf Α ◽  
Infrared Technology

Background: It is known from the most recent literature that far-infrared (FIR) radiations promote a broad spectrum of therapeutic benefits for cells and tissues. Objective: To identify molecular mechanisms by which FIT patches, as a far infrared technology, protects against damage caused by inflammatory process and oxidative stress. Methods: Endothelial cells (HUVEC, Human Umbilical Vein Endothelial Cells) were used as in vitro experimental model. HUVEC were stimulated with a pro-inflammatory cytokine, TNF-α, or hydrogen peroxide (H2O2) to induce oxidative stress. As markers of inflammation were evaluated: VCAM1 (Vascular Cell Adhesion Molecule 1), ICAM1 (Intercellular Adhesion Molecule 1) and E-Selectin by Western Blot analysis. Oxidative stress was assessed by cytofluorimetric analysis. The experiments were performed on control cells (no patch) or in cells treated with the FIT infrared technology applied on the basis of the culture plate. Results: HUVEC stimulated with TNF-α and treated with FIT patches had significant reduction of the expression of VCAM1, ICAM1 and E-Selectin (p<0.05). HUVEC stimulated with H2O2 and treated with FIT patches were significantly protected from oxidative stress (p <0.01) when compared to control cells. We measured cell viability and proliferation in HUVEC and HEK-293 (Human embryonic kidney cells) cells by MTT assay. HEK-293 and HUVEC treated with FIT patches showed a significantly higher percentage of basal vitality compared to control cells (p<0.0001 for HEK-293, p<0.05 for HUVEC). Conclusion: FIT therapy patches - infrared technology, through these protective mechanisms, could be used in all pathologies where an increase in inflammation, oxidative stress and degenerative state are present.

scholarly journals Anti-Inflammatory and Anti-Apoptotic Effects of Stybenpropol A on Human Umbilical Vein Endothelial Cells

2019 ◽  
Vol 20 (21) ◽  
pp. 5383 ◽  
Author(s):  
Li Zhang ◽  
Feifei Wang ◽  
Qing Zhang ◽  
Qiuming Liang ◽  
Shumei Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Umbilical Vein ◽  
Caspase 9 ◽  
Protein Levels ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells ◽  
Cell Adhesion Molecule 1

Inflammation is a key mediator in the progression of atherosclerosis (AS). Benzoinum, a resin secreted from the bark of Styrax tonkinensis, has been widely used as a form of traditional Chinese medicine in clinical settings to enhance cardiovascular function, but the active components of the resin responsible for those pharmaceutical effects remain unclear. To better clarify these components, a new phenylpropane derivative termed stybenpropol A was isolated from benzoinum and characterized via comprehensive spectra a nalysis. We further assessed how this phenylpropane derivative affected treatment of human umbilical vein endothelial cells (HUVECs) with tumor necrosis factor-α (TNF-α). Our results revealed that stybenpropol A reduced soluble intercellular cell adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), interleukin-8 (IL-8), and interleukin-1β (IL-1β) expression by ELISA, inhibited apoptosis, and accelerated nitric oxide (NO) release in TNF-α-treated HUVECs. We further found that stybenpropol A decreased VCAM-1, ICAM-1, Bax, and caspase-9 protein levels, and increased the protein levels of Bcl-2, IKK-β, and IκB-α. This study identified a new, natural phenylpropane derivative of benzoinum, and is the first to reveal its cytoprotective effects in the context of TNF-α-treated HUVECs via regulation of the NF-κB and caspase-9 signaling pathways.

scholarly journals Direct Activation of Human Endothelial Cells by Plasmodium falciparum-Infected Erythrocytes

2005 ◽  
Vol 73 (6) ◽  
pp. 3271-3277 ◽  
Author(s):  
Nicola K. Viebig ◽  
Ulrich Wulbrand ◽  
Reinhold Förster ◽  
Katherine T. Andrews ◽  
Michael Lanzer ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasmodium Falciparum ◽  
Endothelial Cell ◽  
Adhesion Molecule ◽  
Cell Activation ◽  
Physical Contact ◽  
Intercellular Adhesion Molecule ◽  
Immune Reactivity ◽  
Human Endothelial Cells ◽  
Tnf Α

ABSTRACT Cytoadherence of Plasmodium falciparum-infected erythrocytes (PRBC) to endothelial cells causes severe clinical disease, presumably as a of result perfusion failure and tissue hypoxia. Cytoadherence to endothelial cells is increased by endothelial cell activation, which is believed to occur in a paracrine fashion by mediators such as tumor necrosis factor alpha (TNF-α) released from macrophages that initially recognize PRBC. Here we provide evidence that PRBC directly stimulate human endothelial cells in the absence of macrophages, leading to increased expression of adhesion-promoting molecules, such as intercellular adhesion molecule 1. Endothelial cell stimulation by PRBC required direct physical contact for a short time (30 to 60 min) and was correlated with parasitemia. Gene expression profiling of endothelial cells stimulated by PRBC revealed increased expression levels of chemokine and adhesion molecule genes. PRBC-stimulated endothelial cells especially showed increased expression of molecules involved in parasite adhesion but failed to express molecules promoting leukocyte adhesion, such as E-selectin and vascular cell adhesion molecule 1, even after challenge with TNF-α. Collectively, our data suggest that stimulation of endothelial cells by PRBC may have two effects: prevention of parasite clearance through increased cytoadherence and attenuation of leukocyte binding to endothelial cells, thereby preventing deleterious immune reactivity.

scholarly journals Suppressive Effects of the Gynura bicolor Ether Extract on Endothelial Permeability and Leukocyte Transmigration in Human Endothelial Cells Induced by TNF-α

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Shu-Ling Hsieh ◽  
Jyh-Jye Wang ◽  
Kuan-Hua Su ◽  
Ying-Lan Kuo ◽  
Shuchen Hsieh ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Far East ◽  
Endothelial Permeability ◽  
Intercellular Adhesion Molecule ◽  
Ether Extract ◽  
Human Endothelial Cells ◽  
Tnf Α ◽  
Ea.Hy926 Cells ◽  
Gynura Bicolor

Gynura bicolor (Roxb. and Willd.) DC (G. bicolor) is generally used as a dietary vegetable and traditional herb in Taiwan and the Far East. G. bicolor exerts antioxidant and anti-inflammatory effects and regulates blood lipids and cholesterol. However, the effects of G. bicolor on endothelial transmigration and atherosclerosis are not clear. The present study investigated the effects of G. bicolor on endothelial permeability and transmigration in human endothelial cells. We prepared G. bicolor ether extract (GBEE) for use as the experimental material. Under TNF-α stimulation, HL-60 cell adherence to EA.hy926 cells, the shape of EA.hy926 cells, and the expression of adhesion molecules and transmigration-related regulatory molecules were analysed after pretreatment with GBEE for 24 h. GBEE inhibited leukocyte adhesion to endothelial cells, reduced intercellular adhesion molecule-1 (ICAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1) expressions, and decreased endothelial monolayer permeability. GBEE also reduced paracellular transmigration by reducing the levels of reactive oxygen species (ROS), Src phosphorylation, and vascular endothelial-cadherin (VE-cadherin) phosphorylation. GBEE reduced transcellular migration via inhibition of Ras homolog family member A (RhoA) and Rho-associated protein kinase (ROCK) expression and phosphorylation of the ezrin-radixin-moesin (ERM) protein. Incubation of EA.hy926 cells with GBEE for 8 h and stimulation with TNF-α for 3 h reduced the phosphorylation of the inhibitor of kappa B (IĸB) and DNA-binding activity of nuclear factor-ĸB (NF-ĸB). These results suggest that GBEE has a protective effect against endothelial dysfunction via suppression of leukocyte-endothelium adhesion and transmigration.

The Role of Oxidative Stress, Inflammation, and Advanced Glycation End Product in Skin Manifestations of Diabetes Mellitus

2021 ◽  
Vol 17 ◽  
Author(s):  
Lili Legiawati
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Adhesion Molecule ◽  
Intercellular Adhesion Molecule ◽  
Skin Disorders ◽  
Intercellular Adhesion Molecule 1 ◽  
Tnf Α ◽  
Mitogen Activated Protein ◽  
High Level ◽  
Factor Α

: Diabetes mellitus is a metabolic disorder caused by an increase in insulin resistance, a decrease in insulin production, or both of them, resulting in a high level of blood glucose or hyperglycemia. An uncontrolled state of DM may cause complications, namely skin disorder. One or more skin disorders are found amongst 74% of T2DM patients, with the highest percentage is dry skin (47%), followed by infection (10%), diabetic hand (5%), hair loss and diabetic dermopathy (each 4%). In DM, the state of hyperglycemia and production of advanced glycaemic end-products (AGEs) profoundly impact skin changes. In the pathological pathway, AGEs induce oxidative stress and inflammation. Nonetheless, AGEs level is higher in T2DM patients compared to non-T2DM people. This is caused by hyperglycemia and oxidative stress. Binding between AGEs and receptor of AGEs (RAGE) promotes pathway of oxidative stress and inflammation cascade via mitogen-activated protein kinases (MAPK), nuclear factor-k-light-chain-enhancer of activated β cells (NF-kβ), interleukin- 6 (IL-6), tumor necrosis factor-α (TNF-α), expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 2 (VCAM-2) pathway which furtherly effectuates DM complication including skin disorders.

scholarly journals Emerging Roles of Redox-Mediated Angiogenesis and Oxidative Stress in Dermatoses

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Dehai Xian ◽  
Jing Song ◽  
Lingyu Yang ◽  
Xia Xiong ◽  
Rui Lai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Growth Factors ◽  
Molecular Mechanisms ◽  
Capillary Tube ◽  
Proteolytic Enzymes ◽  
Skin Tumor ◽  
Antioxidant Systems ◽  
Antiangiogenic Factors ◽  
And Oxidative Stress

Angiogenesis is the process of new vessel formation, which sprouts from preexisting vessels. This process is highly complex and primarily involves several key steps, including stimulation of endothelial cells by growth factors, degradation of the extracellular matrix by proteolytic enzymes, migration and proliferation of endothelial cells, and capillary tube formation. Currently, it is considered that multiple cytokines play a vital role in this process, which consist of proangiogenic factors (e.g., vascular endothelial growth factor, fibroblast growth factors, and angiopoietins) and antiangiogenic factors (e.g., endostatin, thrombospondin, and angiostatin). Angiogenesis is essential for most physiological events, such as body growth and development, tissue repair, and wound healing. However, uncontrolled neovascularization may contribute to angiogenic disorders. In physiological conditions, the above promoters and inhibitors function in a coordinated way to induce and sustain angiogenesis within a limited period of time. Conversely, the imbalance between proangiogenic and antiangiogenic factors could cause pathological angiogenesis and trigger several diseases. With insights into the molecular mechanisms of angiogenesis, increasing reports have shown that a close relationship exists between angiogenesis and oxidative stress (OS) in both physiological and pathological conditions. OS, an imbalance between prooxidant and antioxidant systems, is a cause and consequence of many vascular complains and serves as one of the biomarkers for these diseases. Furthermore, emerging evidence supports that OS and angiogenesis play vital roles in many dermatoses, such as psoriasis, atopic dermatitis, and skin tumor. This review summarizes recent findings on the role of OS as a trigger of angiogenesis in skin disorders, highlights newly identified mechanisms, and introduces the antiangiogenic and antioxidant therapeutic strategies.

Vascular Protective Effects of Xanthotoxin and Its Action Mechanism in Rat Aorta and Human Vascular Endothelial Cells

2020 ◽  
Vol 57 (6) ◽  
pp. 313-324
Author(s):  
Li-Hua Cao ◽  
Ho Sub Lee ◽  
Zhe-Shan Quan ◽  
Yun Jung Lee ◽  
Yu Jin
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Molecular Mechanisms ◽  
Umbilical Vein ◽  
Neuroprotective Effect ◽  
Intercellular Adhesion Molecule ◽  
Dependent Manner ◽  
Protective Effects ◽  
Concentration Dependent Manner

<b><i>Objective:</i></b> Xanthotoxin (XAT) is a linear furanocoumarin mainly extracted from the plants <i>Ammi majus</i> L. XAT has been reported the apoptosis of tumor cells, anti-convulsant, neuroprotective effect, antioxidative activity, and vasorelaxant effects. This study aimed to investigate the vascular protective effects and underlying molecular mechanisms of XAT. <b><i>Methods:</i></b> XAT’s activity was studied in rat thoracic aortas, isolated with aortic rings, and human umbilical vein endothelial cells (HUVECs). <b><i>Results:</i></b> XAT induced endothelium-dependent vasodilation in a concentration-dependent manner in the isolated rat thoracic aortas. Removal of endothelium or pretreatment of aortic rings with L-NAME, 1<i>H</i>-[1,2,4]-oxadiazolo-[4,3-<i>a</i>]-quinoxalin-1-one, and wortmannin significantly inhibited XAT-induced relaxation. In addition, treatment with thapsigargin, 2-aminoethyl diphenylborinate, Gd<sup>3+</sup>, and 4-aminopyridine markedly attenuated the XAT-induced vasorelaxation. XAT increased nitric oxide production and Akt- endothelial NOS (eNOS) phosphorylation in HUVECs. Moreover, XAT attenuated the expression of TNF-α-induced cell adhesion molecules such as intercellular adhesion molecule, vascular cell adhesion molecule-1, and E-selectin. However, this effect was attenuated by the eNOS inhibitors L-NAME and asymmetric dimethylarginine. <b><i>Conclusions:</i></b> This study suggests that XAT induces vasorelaxation through the Akt-eNOS-cGMP pathway by activating the K<sub>V</sub> channel and inhibiting the L-type Ca<sup>2+</sup> channel. Furthermore, XAT exerts an inhibitory effect on vascular inflammation, which is correlated with the observed vascular protective effects.

scholarly journals Rice‐derived peptide AAGALPS inhibits TNF‐α‐induced inflammation and oxidative stress in vascular endothelial cells

2019 ◽  
Vol 8 (1) ◽  
pp. 659-667 ◽  
Author(s):  
Li‐Tao Tong ◽  
Zhiyuan Ju ◽  
Liya Liu ◽  
Lili Wang ◽  
Xianrong Zhou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Tnf Α ◽  
And Oxidative Stress

scholarly journals The effect of long-term dehydration and subsequent rehydration on markers of inflammation, oxidative stress and apoptosis in the camel kidney

2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Mahmoud A. Ali ◽  
Hassan Abu Damir ◽  
Osman M. Ali ◽  
Naheed Amir ◽  
Saeed Tariq ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Water Conservation ◽  
Mesangial Cells ◽  
Expression Level ◽  
Kidney Cortex ◽  
Mrna Levels ◽  
Sod Activity ◽  
Markers Of Inflammation ◽  
Tnf Α ◽  
Different Response

Abstract Background Dehydration has deleterious effects in many species, but camels tolerate long periods of water deprivation without serious health compromise. The kidney plays crucial role in water conservation, however, some reports point to elevated kidney function tests in dehydrated camels. In this work, we investigated the effects of dehydration and rehydration on kidney cortex and medulla with respect to pro-inflammatory markers, oxidative stress and apoptosis along with corresponding gene expression. Results The cytokines IL-1β and IL-18 levels were significantly elevated in the kidney cortex of dehydrated camel, possibly expressed by tubular epithelium, podocytes and/or mesangial cells. Elevation of IL-18 persisted after rehydration. Dehydration induced oxidative stress in kidney cortex evident by significant increases in MDA and GSH, but significant decreases in SOD and CAT. In the medulla, CAT decreased significantly, but MDA, GSH and SOD levels were not affected. Rehydration abolished the oxidative stress. In parallel with the increased levels of MDA, we observed increased levels of PTGS1 mRNA, in MDA synthesis pathway. GCLC mRNA expression level, involved in GSH synthesis, was upregulated in kidney cortex by rehydration. However, both SOD1 and SOD3 mRNA levels dropped, in parallel with SOD activity, in the cortex by dehydration. There were significant increases in caspases 3 and 9, p53 and PARP1, indicating apoptosis was triggered by intrinsic pathway. Expression of BCL2l1 mRNA levels, encoding for BCL-xL, was down regulated by dehydration in cortex. CASP3 expression level increased significantly in medulla by dehydration and continued after rehydration whereas TP53 expression increased in cortex by rehydration. Changes in caspase 8 and TNF-α were negligible to instigate extrinsic apoptotic trail. Generally, apoptotic markers were extremely variable after rehydration indicating that animals did not fully recover within three days. Conclusions Dehydration causes oxidative stress in kidney cortex and apoptosis in cortex and medulla. Kidney cortex and medulla were not homogeneous in all parameters investigated indicating different response to dehydration/rehydration. Some changes in tested parameters directly correlate with alteration in steady-state mRNA levels.

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