scholarly journals Gamma-tocopherol supplementation ameliorated hyper-inflammatory response during the early cutaneous wound healing in alloxan-induced diabetic mice

2016 ◽  
Vol 242 (5) ◽  
pp. 505-515 ◽  
Author(s):  
Jihyun Shin ◽  
Soo Jin Yang ◽  
Yunsook Lim
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
Inflammatory Response ◽  
Diabetic Control ◽  
Sirtuin 1 ◽  
Nuclear Factor ◽  
Diabetic Mice ◽  
Closure Rate ◽  
Delayed Wound Healing ◽  
Gamma Tocopherol

Delayed wound healing is one of the major diabetic complications. During wound healing process, the early inflammatory stage is important for better prognosis. One of antioxidant nutrient, gamma-tocopherol (GT) is considered to regulate inflammatory conditions. This study investigated the effect of GT supplementation on mechanism associated with inflammation, oxidative stress, and apoptosis during early cutaneous wound healing in diabetic mice. Diabetes was induced by alloxan injection in ICR mice. All mice were divided into three groups: non-diabetic control mice (CON), diabetic control mice (DMC), and diabetic mice supplemented with GT (GT). After two weeks of GT supplementation, excisional wounds were made by biopsy punches (4 mm). Diabetic mice showed increases in fasting blood glucose (FBG) level, hyper-inflammatory response, oxidative stress, and delayed wound closure rate compared to non-diabetic mice. However, GT supplementation reduced FBG level and accelerated wound closure rate by regulation of inflammatory response-related proteins such as nuclear factor kappa B, interleukin-1β, tumor necrosis factor-α, and c-reactive protein, and oxidative stress-related markers including nuclear factor (erythroid derived 2)-like 2, NAD(P)H dehydrogenase quinone1, heme oxygenase-1, manganese superoxide dismutase, catalase and glutathione peroxidase and apoptosis-related markers such as sirtuin-1, peroxisome proliferator-activated receptor gamma coactivator 1- α, and p53 in diabetic mice. Taken together, GT would be a potential therapeutic to prevent diabetes-induced delayed wound healing by regulation of inflammatory response, apoptosis, and oxidative stress. Impact statement Gamma tocopherol has shown ameliorative effect on diabetic wound healing by regulation of inflammation, oxidative stress, and apoptosis demonstrated by nuclear factor kappa B, nuclear factor (erythroid derived 2)-like 2, and sirtuin-1.

scholarly journals Why so little effort to study anti-oxidant therapy in burns?

2016 ◽  
Vol 4 ◽  
pp. 1-2 ◽  
Author(s):  
Gordon L. Klein
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Inflammatory Response ◽  
Burn Injury ◽  
Burn Treatment ◽  
Gamma Tocopherol ◽  
Limited Success ◽  
Anti Oxidant

Abstract Given that oxidative stress is an inherent response to burn injury, it is puzzling as to why investigation into anti-oxidant therapy as an adjunct to burn treatment has been limited. Both the inflammatory response and the stress response to burn injury involve oxidative stress, and there has been some limited success in studies using gamma tocopherol and selenium to improve certain consequences of burns. Much remains to be done to investigate the number, doses and combinations of anti-oxidants, their efficacy, and limitations in improving defined outcomes after burn injury.

scholarly journals Folic Acid Promotes Wound Healing in Diabetic Mice by Suppression of Oxidative Stress

2018 ◽  
Vol 64 (1) ◽  
pp. 26-33 ◽  
Author(s):  
Mei ZHAO ◽  
Jun ZHOU ◽  
Yuan-hua CHEN ◽  
Li YUAN ◽  
Man-man YUAN ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
Folic Acid ◽  
Diabetic Mice

scholarly journals Protective Role of Endogenous Kallistatin in Vascular Injury and Senescence by Inhibiting Oxidative Stress and Inflammation

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Julie Chao ◽  
Youming Guo ◽  
Lee Chao
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Nadph Oxidase ◽  
Vascular Injury ◽  
Oxidase Activity ◽  
Sirtuin 1 ◽  
Mouse Lung ◽  
Heparin Binding ◽  
Diabetic Mice ◽  
Nadph Oxidase Activity

Kallistatin was identified in human plasma as a tissue kallikrein-binding protein and a serine proteinase inhibitor. Kallistatin exerts pleiotropic effects on angiogenesis, oxidative stress, inflammation, apoptosis, fibrosis, and tumor growth. Kallistatin levels are markedly reduced in patients with coronary artery disease, sepsis, diabetic retinopathy, inflammatory bowel disease, pneumonia, and cancer. Moreover, plasma kallistatin levels are positively associated with leukocyte telomere length in young African Americans, indicating the involvement of kallistatin in aging. In addition, kallistatin treatment promotes vascular repair by increasing the migration and function of endothelial progenitor cells (EPCs). Kallistatin via its heparin-binding site antagonizes TNF-α-induced senescence and superoxide formation, while kallistatin’s active site is essential for inhibiting miR-34a synthesis, thus elevating sirtuin 1 (SIRT1)/eNOS synthesis in EPCs. Kallistatin inhibits oxidative stress-induced cellular senescence by upregulating Let-7g synthesis, leading to modulate Let-7g-mediated miR-34a-SIRT1-eNOS signaling pathway in human endothelial cells. Exogenous kallistatin administration attenuates vascular injury and senescence in association with increased SIRT1 and eNOS levels and reduced miR-34a synthesis and NADPH oxidase activity, as well as TNF-α and ICAM-1 expression in the aortas of streptozotocin- (STZ-) induced diabetic mice. Conversely, endothelial-specific depletion of kallistatin aggravates vascular senescence, oxidative stress, and inflammation, with further reduction of Let-7g, SIRT1, and eNOS and elevation of miR-34a in mouse lung endothelial cells. Furthermore, systemic depletion of kallistatin exacerbates aortic injury, senescence, NADPH oxidase activity, and inflammatory gene expression in STZ-induced diabetic mice. These findings indicate that endogenous kallistatin displays a novel role in protection against vascular injury and senescence by inhibiting oxidative stress and inflammation.

scholarly journals Aliskiren Attenuates the Inflammatory Response and Wound Healing Process in Diabetic Mice With Periodontal Disease

2019 ◽  
Vol 10 ◽  
Author(s):  
Sandra Helena Penha Oliveira ◽  
Victor Gustavo Balera Brito ◽  
Sabrina Cruz Tfaile Frasnelli ◽  
Bianca da Silva Ribeiro ◽  
Milena Nunes Ferreira ◽  
...  
Keyword(s):  
Wound Healing ◽  
Inflammatory Response ◽  
Periodontal Disease ◽  
Healing Process ◽  
Wound Healing Process ◽  
Diabetic Mice

scholarly journals Isoliquiritigenin Confers Neuroprotection and Alleviates Amyloid-β42-Induced Neuroinflammation in Microglia by Regulating the Nrf2/NF-κB Signaling

2021 ◽  
Vol 15 ◽  
Author(s):  
Yue Fu ◽  
Jianping Jia
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Molecular Mechanisms ◽  
Morphological Changes ◽  
No Production ◽  
Related Factor ◽  
Nuclear Factor ◽  
Qrt Pcr ◽  
Bv2 Cells ◽  
And Oxidative Stress

BackgroundNeuroinflammation and oxidative stress are two major pathological characteristics of Alzheimer’s disease (AD). Amyloid-β oligomers (AβO), a toxic form of Aβ, promote the neuroinflammation and oxidative stress in the development of AD. Isoliquiritigenin (ISL), a natural flavonoid isolated from the root of liquorice, has been shown to exert inhibitory effects on inflammatory response and oxidative stress.ObjectivesThe main purpose of this study is to assess the influence of ISL on inflammatory response and oxidative stress in BV2 cells stimulated with AβO, and to explore the underlying molecular mechanisms.Methods3-(4,5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H- tetrazolium bromide (MTT) and lactate dehydrogenase (LDH) cytotoxicity assays were used to assess the toxic or protective effects of ISL. The expression levels of interleukin-1β, interleukin-6, and tumor necrosis factor-α were assessed by quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assays. Morphological changes in BV2 cells were assessed by immunofluorescence method. Nitric oxide (NO) assay kit was used to determinate the NO production. Western blot, qRT-PCR and immunofluorescence were used to explore the underlying molecular mechanisms.ResultsISL treatment reduced the production of inflammatory cytokines and NO, and alleviated the morphological changes in BV2 cells induced by AβO. ISL treatment further protected N2a cells from the toxic medium of AβO-stimulated BV2 cells. ISL activated nuclear factor erythroid-2 related factor 2 (Nrf2) signaling and suppressed nuclear factor-κB (NF-κB) signaling in BV2 cells.ConclusionISL suppresses AβO-induced inflammation and oxidative stress in BV2 cells via the regulation of Nrf2/NF-κB signaling. Therefore, ISL indirectly protects neurons from the damage of toxic conditioned media.

136A: ALTERATION OF THE INFLAMMATORY RESPONSE WITH HOXB3 ADMINISTRATION ACCELERATES WOUND HEALING IN DIABETIC MICE

2010 ◽  
Vol 125 (Supplement) ◽  
pp. 91
Author(s):  
KA Belek ◽  
AA Dunn ◽  
M Kuri ◽  
DM Young ◽  
N Boudreau
Keyword(s):  
Wound Healing ◽  
Inflammatory Response ◽  
Diabetic Mice
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