scholarly journals Cloves Regulate Na+-K+-ATPase to Exert Antioxidant Effect and Inhibit UVB Light-Induced Skin Damage in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Xi Gao ◽  
Fuling Luo ◽  
Hengguang Zhao
Keyword(s):  
Oxidative Stress ◽  
Mouse Skin ◽  
The Body ◽  
Muscle Membrane ◽  
Composition Analysis ◽  
Syzygium Aromaticum ◽  
Skin Damage ◽  
Stress Injury ◽  
Inflammatory Damage ◽  
Tnf Α

The purpose of this study was to observe the effect of cloves (Syzygium aromaticum (L.) Merr. & L.M. Perry) on the mouse skin using a UVB-induced skin injury mouse model. The serum, liver, and skin indexes of mice were determined by kits, H&E tissue staining, and qPCR assay. The compound composition of cloves was determined by HPLC. The results showed that cloves increased the activity of Na+-K+-ATPase in the skin and then maintained the sodium and potassium pump in the damaged skin muscle membrane. Cloves alleviated the oxidative stress injury induced by UVB irradiation by normalizing the related oxidative stress indexes (T-SOD, CAT, AGEs, and H2O2) in serum and skin. Inhibition of the proinflammatory cytokines TNF-α, IL-1β, and IL-6 and increased activation of anti-inflammatory cytokines IL-4 and IL-10 occurred after treatment with cloves, which ultimately reduced the inflammatory damage to the body. Further results showed that cloves upregulate SOD1, SOD2, CAT, GSH, IL-10, IκB-α, AMPK, SIRT1, LKB1, PGC-1α, APPL1, and FoxO1 and downregulate NF-κB p65, TNF-α, IL-6, and mTOR mRNA expression in the skin tissues of UVB-damaged mice. The results of composition analysis showed that the five most abundant compounds in cloves are rutin, isoquercitrin, ferulic acid, dihydroquercetin, and quercitrin. Cloves regulate the skin sarcomembrane Na+-K+-ATPase through these five compounds, and because they regulate the oxidation, inflammation, and ATP energy consumption of the body, they subsequently protect the skin from UVB damage.

Abstract 1125: Mulberry Leaf Ameliorates The Production Of Adipocytokines By Inhibiting Oxidative Stress In White Adipose Tissue In db/db Mice

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Masayuki Sugimoto ◽  
Hidenori Arai ◽  
Yukinori Tamura ◽  
Toshinori Murayama ◽  
Koh Ono ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Metabolic Disorders ◽  
The Body ◽  
Mulberry Leaf ◽  
The Metabolic Syndrome ◽  
Pparγ Agonist ◽  
Tnf Α

Mulberry leaf (ML) is commonly used to feed silkworms. Previous study showed that ML ameliorates atherosclerosis. However, its mechanism is not completely understood. Because dysregulated production of adipocytokines is involved in the development of the metabolic syndrome and cardiovascular disease, we examined the effect of ML on the production of adipocytokines and metabolic disorders related to the metabolic syndrome, and compared its effect with that of a PPARγ agonist, pioglitazone (Pio). By treating obese diabetic db/db mice with ML, Pio, and their combination, we investigated the mechanism by which they improve metabolic disorders. In this study, db/+m (lean control) and db/db mice were fed a standard diet with or without 3% (w/w) ML and/or 0.01% (w/w) Pio for 12 weeks from 9 weeks of age. At the end of the experiment we found that ML decreased plasma glucose and triglyceride by 32% and 30%, respectively. Interestingly, administration of ML in addition to Pio showed additive effects; further 40% and 30% reduction in glucose and triglyceride compared with Pio treatment, respectively. Moreover, administration of ML in addition to Pio suppressed the body weight increase by Pio treatment and reduced visceral/subcutaneous fat ratio by 20% compared with control db/db mice. Importantly, ML treatment increased expression of adiponectin in white adipose tissue (WAT) by 40%, which was only found in db/db mice, not in control db/+m mice. Combination of ML and Pio increased plasma adiponectin concentrations by 25% and its expression in WAT by 17% compared with Pio alone. In contrast, ML decreased expression of TNF-α and MCP-1 by 25% and 20%, respectively, and the addition of Pio resulted in a further decrease of these cytokines by about 45%. To study the mechanism, we examined the role of oxidative stress. ML decreased the amount of lipid peroxides by 43% and the expression of NADPH oxidase subunits in WAT, which was consistent with the results of TNF-α and MCP-1. Thus our results indicate that ML ameliorates adipocytokine dysregulation by inhibiting oxidative stress in WAT of obese mice, and that ML may have a potential for the treatment of the metabolic syndrome as well as reducing adverse effects of Pio.

scholarly journals Andrographis paniculata and Its Bioactive Diterpenoids Protect Dermal Fibroblasts against Inflammation and Oxidative Stress

Antioxidants ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 432 ◽  
Author(s):  
Eugenie Mussard ◽  
Sundy Jousselin ◽  
Annabelle Cesaro ◽  
Brigitte Legrain ◽  
Eric Lespessailles ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dermal Fibroblasts ◽  
Andrographis Paniculata ◽  
Type I ◽  
Ros Production ◽  
Skin Damage ◽  
Aging Effects ◽  
Natural Treatment ◽  
Tnf Α

Andrographis paniculata (Burm.f.) has long been used in ayurvedic medicine through its anti-inflammatory properties. However, its protective effect of skin aging has not been studied in vitro. This study aimed to investigate the anti-aging effects of methanolic extract (ME), andrographolide (ANDRO), neoandrographolide (NEO), 14-deoxyandrographolide (14DAP) and 14-deoxy-11,12-didehydroandrographolide (14DAP11-12) on human dermal fibroblasts (HDFa) under pro-oxidant or pro-inflammatory condition. The in vitro anti-aging capacity of ME, ANDRO, NEO, 14DAP, and 14DAP11-12 (1, 2.5 and 5 µg/mL) was performed in HDFa. Oxidative stress and inflammation were induced by hydrogen peroxide and lipopolysaccharide/TNF-α, respectively. Reactive oxygen species (ROS) production was measured by the fluorescence of DCF-DA probe and cytokines were quantified by ELISA (IL6 and IL8) or RTqPCR (TNF-α). Procollagen type I production was determined by an ELISA. Our results showed a decrease in ROS production with ME and 14DAP at 5 µg/mL and 1 µg/mL, respectively. Furthermore, IL-6 production and TNF-α expression decreased under ANDRO and ME at 5 µg/mL. Our data indicated that ME and 14DAP protect from oxidative stress. Additionally, ME and ANDRO decreased an inflammation marker, IL-6. This suggests their potential natural treatment against skin damage. Hence, their applications could be of interest in cosmetics for preventing skin ageing.

scholarly journals Bone marrow mesenchymal stem cells stimulated by tumor necrosis factor-α can promote the repair of fatty liver cell oxidative stress injury and fatty liver ischemia-reperfusion injury

2021 ◽  
Author(s):  
Yuying Tan ◽  
Jiali Qiu ◽  
Weiqi Zhang ◽  
Yan Xie ◽  
Chiyi Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Fatty Liver ◽  
Liver Cell ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Tnf Α

Mesenchymal stem cells (MSCs) have great prospects for the treatment of ischemia-reperfusion injury (IRI) after liver transplantation. At this stage, the main factor limiting MSCs in the treatment of fatty liver IRI of the donor liver is the residence time of stem cells at the site of inflammatory injury. This study investigated whether bone marrow mesenchymal stem cells (BMSCs) stimulated by tumor necrosis factor-α (TNF-α) can promote the repair of fatty liver cell oxidative stress injury and fatty liver IRI in rats. The results indicated the BMSCs treatment group stimulated by TNF-α had lower indexes and significantly improved oxidative stress damage in vitro through Transwell chamber co-culture experiment, compared with the control group. In vivo, compared with the PBS group and the BMSCs group, the indexes of the BMSCs treatment group stimulated by TNF-α were reduced, and the degree of tissue damage was significantly reduced. BMSCs can repair fatty liver cell oxidative stress injury and fatty liver IRI, however, BMSCs stimulated by TNF-α can promote the repair of tissues and cells.

scholarly journals Protective Effect of Polymethoxyflavones Isolated from Kaempferia parviflora against TNF-α-Induced Human Dermal Fibroblast Damage

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1609
Author(s):  
Hung Manh Phung ◽  
Sullim Lee ◽  
Sukyung Hong ◽  
Sojung Lee ◽  
Kiwon Jung ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Mitogen Activated Protein Kinase ◽  
Type I ◽  
Skin Damage ◽  
Kaempferia Parviflora ◽  
Matrix Metalloproteinase 1 ◽  
Tnf Α

Similar to other organs, the skin undergoes a natural aging process. Moreover, constant direct exposure to environmental stresses, including ultraviolet irradiation, causes the signs of skin aging to appear rather early. Reactive oxygen species (ROS) and inflammatory responses accelerate skin damage in extrinsic aging. In this study, we aimed to investigate the skin protective effects of polymethoxyflavones found in Kaempferia parviflora against oxidative stress and inflammation-induced damage in human dermal fibroblasts (HDFs) stimulated by tumor necrosis factor-α (TNF-α). The experimental data identified 5,7,4′ trimethoxyflavone (TMF) as the most potent constituent in preventing TNF-α-induced HDF damage among the tested compounds and it was not only effective in inhibiting matrix metalloproteinase-1 (MMP-1) production but also in stimulating collagen, type I, and alpha 1 (COLIA1) expression. TMF suppressed TNF-α-stimulated generation of ROS and pro-inflammatory mediators, such as cyclooxygenase-2 (COX-2), interleukin (IL)-1β, and IL-6 in HDFs. TMF also inhibited the pathways regulating fibroblast damage, including mitogen-activated protein kinase (MAPK), activator protein 1 (AP-1), and nuclear factor-kappa B (NF-κB). In conclusion, TMF may be a potential agent for preventing skin aging and other dermatological disorders associated with oxidative stress and inflammation.

scholarly journals Oenanthe Javanica Extract Protects Mouse Skin from UVB Radiation via Attenuating Collagen Disruption and Inflammation

2019 ◽  
Vol 20 (6) ◽  
pp. 1435 ◽  
Author(s):  
Young Her ◽  
Bich-Na Shin ◽  
Yun Lee ◽  
Joon Park ◽  
Dae Kim ◽  
...  
Keyword(s):  
Mouse Skin ◽  
Type Iii Collagen ◽  
Type I ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Protein Levels ◽  
Photodamaged Skin ◽  
Tnf Α ◽  
Oenanthe Javanica ◽  
Cox 2

In recent years, the use of botanical agents to prevent skin damage from solar ultraviolet (UV) irradiation has received considerable attention. Oenanthe javanica is known to exert anti-inflammatory and antioxidant activities. This study investigated photoprotective properties of an Oenanthe javanica extract (OJE) against UVB-induced skin damage in ICR mice. The extent of skin damage was evaluated in three groups: control mice with no UVB, UVB-exposed mice treated with vehicle (saline), and UVB-exposed mice treated with 1% extract. Photoprotective properties were assessed in the dorsal skin using hematoxylin and eosin staining, Masson trichrome staining, immunohistochemical staining, quantitative real-time polymerase chain reaction, and western blotting to analyze the epidermal thickness, collagen expression, and mRNA and protein levels of type I collagen, type III collagen, and interstitial collagenases, including matrix metalloproteinase (MMP)-1 and MMP-3. In addition, tumor necrosis factor (TNF)-α and cyclooxygenase (COX)-2 protein levels were also assessed. In the UVB-exposed mice treated with extract, UV-induced epidermal damage was significantly ameliorated. In this group, productions of collagen types I and III were increased, and expressions of MMP-1 and MMP-3 were decreased. In addition, TNF-α and COX-2 expressions were reduced. Based on these findings, we conclude that OJE displays photoprotective effects against UVB-induced collagen disruption and inflammation and suggest that Oenanthe javanica can be used as a natural product for the treatment of photodamaged skin.

scholarly journals A Brief Overview of Oxidative Stress in Adipose Tissue with a Therapeutic Approach to Taking Antioxidant Supplements

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 594
Author(s):  
Shima Taherkhani ◽  
Katsuhiko Suzuki ◽  
Ruheea Taskin Ruhee
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Animal Studies ◽  
The Body ◽  
Fast Foods ◽  
Tnf Α ◽  
Excessive Consumption ◽  
Antioxidant Supplements ◽  
Factor Α ◽  
Necrosis Factor

One of the leading causes of obesity associated with oxidative stress (OS) is excessive consumption of nutrients, especially fast-foods, and a sedentary lifestyle, characterized by the ample accumulation of lipid in adipose tissue (AT). When the body needs energy, the lipid is broken down into glycerol (G) and free fatty acids (FFA) during the lipolysis process and transferred to various tissues in the body. Materials secreted from AT, especially adipocytokines (interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α)) and reactive oxygen species (ROS), are impressive in causing inflammation and OS of AT. There are several ways to improve obesity, but researchers have highly regarded the use of antioxidant supplements due to their neutralizing properties in removing ROS. In this review, we have examined the AT response to OS to antioxidant supplements focusing on animal studies. The results are inconsistent due to differences in the study duration and diversity in animals (strain, age, and sex). Therefore, there is a need for different studies, especially in humans.

scholarly journals Oxidative stress and ageing: is ageing a cysteine deficiency syndrome?

2005 ◽  
Vol 360 (1464) ◽  
pp. 2355-2372 ◽  
Author(s):  
Wulf Dröge
Keyword(s):  
Oxidative Stress ◽  
Insulin Receptor ◽  
Biological Tissues ◽  
Deficiency Syndrome ◽  
The Body ◽  
Immune Functions ◽  
Insulin Receptor Signalling ◽  
Tnf Α ◽  
Insulin Responsiveness ◽  
Factor Α

Reactive oxygen species (ROS) are constantly produced in biological tissues and play a role in various signalling pathways. Abnormally high ROS concentrations cause oxidative stress associated with tissue damage and dysregulation of physiological signals. There is growing evidence that oxidative stress increases with age. It has also been shown that the life span of worms, flies and mice can be significantly increased by mutations which impede the insulin receptor signalling cascade. Molecular studies revealed that the insulin-independent basal activity of the insulin receptor is increased by ROS and downregulated by certain antioxidants. Complementary clinical studies confirmed that supplementation of the glutathione precursor cysteine decreases insulin responsiveness in the fasted state. In several clinical trials, cysteine supplementation improved skeletal muscle functions, decreased the body fat/lean body mass ratio, decreased plasma levels of the inflammatory cytokine tumour necrosis factor α (TNF-α), improved immune functions, and increased plasma albumin levels. As all these parameters degenerate with age, these findings suggest: (i) that loss of youth, health and quality of life may be partly explained by a deficit in cysteine and (ii) that the dietary consumption of cysteine is generally suboptimal and everybody is likely to have a cysteine deficiency sooner or later.

scholarly journals Oxidative Stress and Inflammation, MicroRNA, and Hemoglobin Variations after Administration of Oxygen at Different Pressures and Concentrations: A Randomized Trial

2021 ◽  
Vol 18 (18) ◽  
pp. 9755
Author(s):  
Gerardo Bosco ◽  
Matteo Paganini ◽  
Tommaso Antonio Giacon ◽  
Alberto Oppio ◽  
Alessandra Vezzoli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Renal Function ◽  
The Body ◽  
Oxygen Species ◽  
Protective Mechanisms ◽  
Neopterin Concentration ◽  
Tnf Α ◽  
Reduced State

Exercise generates reactive oxygen species (ROS), creating a redox imbalance towards oxidation when inadequately intense. Normobaric and hyperbaric oxygen (HBO) breathed while not exercising induces antioxidant enzymes expression, but literature is still poor. Twenty-two athletes were assigned to five groups: controls; 30%, or 50% O2; 100% O2 (HBO) at 1.5 or 2.5 atmosphere absolute (ATA). Twenty treatments were administered on non-training days. Biological samples were collected at T0 (baseline), T1 (end of treatments), and T2 (1 month after) to assess ROS, antioxidant capacity (TAC), lipid peroxidation, redox (amino-thiols) and inflammatory (IL-6, 10, TNF-α) status, renal function (i.e., neopterin), miRNA, and hemoglobin. At T1, O2 mixtures and HBO induced an increase of ROS, lipid peroxidation and decreased TAC, counterbalanced at T2. Furthermore, 50% O2 and HBO treatments determined a reduced state in T2. Neopterin concentration increased at T1 breathing 50% O2 and HBO at 2.5 ATA. The results suggest that 50% O2 treatment determined a reduced state in T2; HBO at 1.5 and 2.5 ATA similarly induced protective mechanisms against ROS, despite the latter could expose the body to higher ROS levels and neopterin concentrations. HBO resulted in increased Hb levels and contributed to immunomodulation by regulating interleukin and miRNA expression.

scholarly journals Oxidative Stress Mediates UVC-Induced Increases in Epidermal Autofluorescence of C57 Mouse Ears

2018 ◽  
Author(s):  
Mingchao Zhang ◽  
Dhruba Tara Maharjan ◽  
Yujia Li ◽  
Weihai Ying
Keyword(s):  
Oxidative Stress ◽  
Significant Role ◽  
Cysteine Protease ◽  
The Body ◽  
Skin Damage ◽  
Multiple Regions ◽  
Acetyl Cysteine ◽  
Keratin 1

AbstractOur recent study has reported that UV-induced epidermal autofluorescence (AF) can be used as a novel biomarker for predicting UV-induced skin damage, which is originated from UV-induced, cysteine protease-mediated keratin 1 degradation. A key question regarding these findings is: Does oxidative stress play a significant role in the UV-induced epidermal AF and keratin 1 proteolysis? In our current study, we administered the widely used antioxidant N-acetyl cysteine (NAC) into the skin of mouse ears to test our hypothesis that oxidative stress mediates UV-induced increases in the epidermal AF and keratin 1 degradation. Our study has shown that NAC administration can significantly attenuate the UVC-induced AF increases. The NAC administration can also significantly decrease the UVC-induced keratin 1 degradation. Collectively, our findings have indicated that the oxidative stress induced by UVC is causative to the UVC-induced increases in epidermal AF and keratin 1 proteolysis. Moreover, since oxidative stress is significantly increased in multiple regions of the body in several major diseases, the oxidative stress-induced increases in epidermal AF may become a novel biomarker for diagnosis of major diseases.

Ethanol consumption increases renal dysfunction and mortality in a mice model of sub-lethal sepsis

2020 ◽  
Author(s):  
Gabriel T. Do Vale ◽  
Sthefany Teodoro Ricci ◽  
Alessandra Oliveira Silva ◽  
Carlos Renato Tirapelli ◽  
Carla Speroni Ceron
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Renal Dysfunction ◽  
Catalase Activity ◽  
Cecal Ligation ◽  
Ethanol Consumption ◽  
Chronic Ethanol ◽  
Inflammatory Damage ◽  
Chronic Ethanol Consumption ◽  
Tnf Α

Chronic ethanol consumption and sepsis cause oxidative stress and renal dysfunction. This study aimed to examine whether chronic ethanol consumption sensitizes the mice kidney to sub-lethal cecal ligation and puncture (SL-CLP) sepsis, leading to impairment of renal function by tissue oxidative and inflammatory damage. Male C57BL/6J mice were treated for 9 weeks with ethanol (20% v/v), before SL-CLP was induced. Systolic blood pressure (SBP), survival rate, plasma creatinine, oxidative stress and inflammatory parameters, iNOS, cytokines, metalloproteinases (MMPs) and theirs tissue inhibitors (TIMPs) were evaluated. Chronic ethanol consumption increased SBP, creatinine levels, O<sub>2</sub><sup>.</sup><sup>−</sup> and H<sub>2</sub>O<sub>2</sub> levels, lipid peroxidation, catalase activity, Nox4, IL-6 and TNF-α levels, and MMP-9/TIMP-1 ratio. SL-CLP decreased SBP, increased creatinine levels, lipid peroxidation, IL-6, TNF-α, nitrate/nitrite (NOx) and iNOS levels, and MMP-2/TIMP-2 ratio, and decreased catalase activity. SL-CLP mice previously treated with ethanol showed a similar decrease in SBP, but higher mortality and creatinine levels than SL-CLP alone. These responses were mediated by increased O<sub>2</sub><sup>.</sup><sup>−</sup>, lipid peroxidation, IL-6, TNF-α, NOx, iNOS, MMP-2 and MMP-9 levels, and MMP-9/TIMP-1 and MMP-2/TIMP-2 ratios. Our findings demonstrated that previous oxidative stress and inflammatory damage caused by ethanol consumption sensitizes the kidney to SL-CLP injury, resulting in impaired kidney function and sepsis prognosis.

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