• 제목/요약/키워드: oxidative regeneration

검색결과 40건 처리시간 0.025초

Tetrahydropteridines possess antioxidant roles to guard against glucose-induced oxidative stress in Dictyostelium discoideum

  • Park, Seon-Ok;Kim, Hye-Lim;Lee, Soo-Woong;Park, Young Shik
    • BMB Reports
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    • 제46권2호
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    • pp.86-91
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    • 2013
  • Glucose effects on the vegetative growth of Dictyostelium discoideum Ax2 were studied by examining oxidative stress and tetrahydropteridine synthesis in cells cultured with different concentrations (0.5X, 7.7 g $L^{-1}$; 1X, 15.4 g $L^{-1}$; 2X, 30.8 g $L^{-1}$) of glucose. The growth rate was optimal in 1X cells (cells grown in 1X glucose) but was impaired drastically in 2X cells, below the level of 0.5X cells. There were glucose-dependent increases in reactive oxygen species (ROS) levels and mitochondrial dysfunction in parallel with the mRNA copy numbers of the enzymes catalyzing tetrahydropteridine synthesis and regeneration. On the other hand, both the specific activities of the enzymes and tetrahydropteridine levels in 2X cells were lower than those in 1X cells, but were higher than those in 0.5X cells. Given the antioxidant function of tetrahydropteridines and both the beneficial and harmful effects of ROS, the results suggest glucose-induced oxidative stress in Dictyostelium, a process that might originate from aerobic glycolysis, as well as a protective role of tetrahydropteridines against this stress.

CDDO-Me alleviates oxidative stress in human mesenchymal stem cells

  • Cho, Hye Jin;Kim, Tae Min
    • 한국동물생명공학회지
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    • 제36권4호
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    • pp.285-291
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    • 2021
  • Mesenchymal stem cells (MSCs) have been recognized as a therapeutic tool for various diseases due to its unique ability for tissue regeneration and immune regulation. However, poor survival during in vitro expansion and after being administrated in vivo limits its clinical uses. Accordingly, protocols for enhancing cell survivability is critical for establishing an efficient cell therapy is needed. CDDO-Me is a synthetic C-28 methyl ester of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid, which is known to stimulate nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway. Herein, report that CDDO-Me promoted the proliferation of MSCs and increased colony forming units (CFU) numbers. No alteration in differentiation into tri-lineage mesodermal cells was found after CDDO-Me treatment. We observed that CDDO-Me treatment reduced the cell death induced by oxidative stress, demonstrated by the augment in the expression of Nrf2-downstream genes. Lastly, CDDO-Me led to the nuclear translocation of NRF2. Our data indicate that CDDO-Me can enhance the functionality of MSCs by stimulating cell survival and increasing viability under oxidative stress.

Celecoxib의 항산화 작용에 따른 성체 치주인대 줄기세포 사멸억제 (Inhibition of Human Periodontal Stem Cell Death Following the Antioxidant Action of Celecoxib)

  • 이경희
    • 대한통합의학회지
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    • 제11권2호
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    • pp.169-179
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    • 2023
  • Purpose : Although human periodontal ligament stem cells (hPDLSCs) are a supportive factor for tissue engineering, oxidative stress during cell culture and transplantation has been shown to affect stem cell viability and mortality, leading to failed regeneration. The aim of this study was to evaluate the antioxidant and protective effects against cell damage of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, and the antioxidant signal of hPDLSCs in H2O2-induced oxidative stress. Methods : To induce oxidative stress in cultured hPDLSCs, H2O2 was used as an exogenous reactive oxygen species (ROS). Dose-dependent celecoxib (.1, 1, 10, or 100 µM) was administered after H2O2 treatment. WST-1 assay was used to assess cell damage and western blot was used to observe antioxidant activity of hPDLSCs in oxidative stress. Immunohistochemistry was performed for inverting the localization of the SOD and Nrf2 antibody. Results : We found that progressive cell death was induced in hPDLSCs by H2O2 treatment. However, low-dose celecoxib reduced H2O2-induced cellular damage and eventually enhanced the SOD activity and Nrf2 signal of hPDLSCs. Oxidative stress-induced morphological change in hPDLSCs included lowered the survival and number of spindle-shaped cells, and shrinkage and shortening of cell fibers. Notably, celecoxib promoted cell survival function and activated antioxidants such as SOD and Nrf2 by positively regulating the cell survival signal pathway, and also reduced the number of morphological changes in hPDLS. Immunohistochemistry results showed a greater number of SOD- and Nrf2-stained cells in the celecoxib-treated group following oxidative stress. Conclusion : By increasing SOD and Nrf2 expression at the antioxidant system, the findings suggest that celecoxib enhanced the antioxidative ability of hPDLSCs and protected cell viability against H2O2-induced oxidative stress by increasing SOD and Nrf2 expression in the antioxidant system.

The Establishment of Tumor Necrosis Factor Receptor-associated Protein1 (TRAP1) Transgenic Mice and Severe Fat Accumulation in the Liver of TRAP1 Mice during Liver Regeneration

  • Im, Chang-Nim;Zheng, Ying;Kim, Sun Hye;Huang, Tai-Qin;Cho, Du-Hyong;Seo, Jeong-Sun
    • Interdisciplinary Bio Central
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    • 제5권4호
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    • pp.9.1-9.7
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    • 2013
  • Introduction: Tumor necrosis factor receptor-associated protein 1 (TRAP1) is a mitochondrial heat shock protein (HSP), which belongs to HSP90 family. It plays important roles in regulating mitochondrial integrity, protecting against oxidative stress, and inhibiting cell death. Recent studies suggest that TRAP1 is linked to mitochondria and its metabolism. In this study, we established TRAP1 transgenic mice and performed partial hepatectomy (PH) on wild-type (WT) and TRAP1 transgenic mice to investigate the function of TRAP1 during liver regeneration. Results and Discussion: We found that TRAP1 was highly expressed in liver as well as kidney. In addition, liver regeneration slightly decreased together with increased fatty liver and inflammation at 72 hr after PH in TRAP1 transgenic mice compared with WT control group mice. Concomitantly, we observed decreased levels of p38 protein in TRAP1 transgenic mice compared with WT control group mice. These results suggest that TRAP1 plays a critical role in liver energy balance by regulating lipid accumulation during liver regeneration. Conclusions and Prospects: To our knowledge, we reported, for the first time, that liver regeneration slightly reduced together with increased fat accumulations after PH in TRAP1 transgenic mice compared with WT control group mice. Concomitantly, we observed decreased levels of p38 protein in TRAP1 transgenic mice compared with WT control group mice. Overexpression of TRAP1 might affect liver regeneration via disturbing mitochondrial function leading to fatty liver in vivo.

Application of a Novel Carbon Regeneration Process for Disposal of APEG Treatment Waste

  • 류건상;Shubender Kapila
    • Bulletin of the Korean Chemical Society
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    • 제18권8호
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    • pp.814-818
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    • 1997
  • The chemical waste treatment, APEG (alkali/polyethylene glycol) process has been shown to be effective for the dechlorination of PCBs in transformer oil. Considerable amount of PCBs, however, still remains in the waste exceeding the 25-50 ppm limit set by regulatory agency. A new thermal regeneration technology has been developed in our laboratory for disposal of hazardous organic wastes. Due to the limited oxidation of carbon surface through the reverse movement of flame front to oxidant flow, this technology was termed counterflow oxidative system (COS). Specially, the oxidant flow in the COS process is a principal parameter which determines the optimum conditions regarding acceptable removal and destruction efficiency of adsorbed organic wastes at minimal carbon loss. The COS process, under optimum conditions, was found to be very effective and the removal and destruction efficiency of 99.99% or better was obtained for residual PCBs in the waste while bulk (≥90%) of carbon was recovered. Any toxic formation of polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzo furans (PCDFs) were not detected in the regenerated carbon and impinger traps. The results of surface area measurement showed that the adsorptive property of regenerated carbon is mostly reclaimed during the COS process.

Endothelial cell autophagy in the context of disease development

  • Basheer Abdullah Marzoog
    • Anatomy and Cell Biology
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    • 제56권1호
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    • pp.16-24
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    • 2023
  • Endothelial cells (EC) are the anatomical boundaries between the intravascular and extravascular space. Damage to ECs is catastrophic and induces endothelial cell dysfunction. The pathogenesis is multifactorial and involves dysregulation in the signaling pathways, membrane lipids ratio disturbance, cell-cell adhesion disturbance, unfolded protein response, lysosomal and mitochondrial stress, autophagy dysregulation, and oxidative stress. Autophagy is a lysosomal-dependent turnover of intracellular components. Autophagy was recognized early in the pathogenesis of endothelial dysfunction. Autophagy is a remarkable patho (physiological) process in the cell homeostasis regulation including EC. Regulation of autophagy rate is disease-dependent and impaired with aging. Up-regulation of autophagy induces endothelial cell regeneration/differentiation and improves the function of impaired ones. The paper scrutinizes the molecular mechanisms and triggers of EC dysregulation and current perspectives for future therapeutic strategies by autophagy targeting.

Effect of Allopurinol on the Ethanol-induced Oxidative Stress : Mechanism of Allopurinol Action

  • Park, Min-Kyung
    • Preventive Nutrition and Food Science
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    • 제3권1호
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    • pp.48-55
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    • 1998
  • An acute ethanol load(50mmol/kg , i.p) resulted in an increase in peroxidation and a decrease in the levels of $\alpha$-tocopherol and ascorbate in rat cerebellum. Pretreatement with allopurinol(146$\mu$mol/kg, i.p) prevented the ethnol-induced increment in lipid peroxidation and decrease in $\alpha$-tocopherol content. However, the decrease of ascorbate was of greater magnitude when allopurinol was associated with ethanol. These results suggested that allopurinol. besides its action as a radical scavenger and xanthine oxidase inhibitor, might favor the regeneration of $\alpha$-tocopherol antioxidant acitviity was studied using ${\gamma}$-radiolysis in aerated ethanolic solutions. Even though allopurinol did not react by itself with $\alpha$-hydroxyethyl-peroxyl radicals [H3C-CH(OH)OO] , it enhance the $\alpha$-hydroxyethyl-peroxyl radical scavenging properties of $\alpha$tocopherol. The regeneration of $\alpha$-tocopherol from the $\alpha$-hydroxyethyl-peroxyl radical scavenging properties of $\alpha$-tocophero. The regeneration of $\alpha$-tocopherol from the $\alpha$-tocopherol radical by ascorbate remained as efficient in the presence of allopurinol as in its absence. The effects of allopurinol on the Vitamin E oxidation-reduction mechanism could be involoved in the beneficial effectof allopurinol on the biological cellular damages linked to free radical reactions.

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Tree of life: endothelial cell in norm and disease, the good guy is a partner in crime!

  • Basheer Abdullah Marzoog
    • Anatomy and Cell Biology
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    • 제56권2호
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    • pp.166-178
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    • 2023
  • Undeniably, endothelial cells (EC) contribute to the maintenance of the homeostasis of the organism through modulating cellular physiology, including signaling pathways, through the release of highly active molecules as well as the response to a myriad of extrinsic and intrinsic signaling factors. Review the data from the current literature on the EC role in norm and disease. Endothelium maintains a precise balance between the released molecules, where EC dysfunction arises when the endothelium actions shift toward vasoconstriction, the proinflammatory, prothrombic properties after the alteration of nitric oxide (NO) production and oxidative stress. The functions of the EC are regulated by the negative/positive feedback from the organism, through EC surface receptors, and the crosstalk between NO, adrenergic receptors, and oxidative stress. More than a hundred substances can interact with EC. The EC dysfunction is a hallmark in the emergence and progression of vascular-related pathologies. The paper concisely reviews recent advances in EC (patho) physiology. Grasping EC physiology is crucial to gauge their potential clinical utility and optimize the current therapies as well as to establish novel nanotherapeutic molecular targets include; endothelial receptors, cell adhesion molecules, integrins, signaling pathways, enzymes; peptidases.

DA-3711:A POTENT TISSUE-ENGINEERED ACTIVE INGREDIENTS FOR ANTI-AGING

  • Kim, B. M.;Lee, M.;Lee, J. H.;I. S. Doo;M. K. Son;S. H. Kang;Kim, W. B.;J. W. Kwon
    • 대한화장품학회:학술대회논문집
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    • 대한화장품학회 2003년도 IFSCC Conference Proceeding Book I
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    • pp.659-659
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    • 2003
  • In this study, we have investigated the potent anti-aging effect of DA-3711, a cosmetic ingredient derived from artificial skin culture. The artificial skin was originally developed as a skin replacement for the treatment of chronic skin wounds. To produce DA-3711, neonatal human fibroblasts were seeded into biocompatible collagen/chitosan/glycosaminoglycan (GAG) scaffolds and cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with fetal bovine serum and nonessential amino acids. Analysis of the culture broth (DA-3711) showed that growth factors such as VEGF, TGF-$\beta$, KGF were present at significantly higher levels that in the culture broth of fibroblasts cultured in monolayer. The biological activity of DA-3711 was assessed by measuring in vitro cell proliferation and collagen synthesis of normal human fibroblasts. Fibroblasts treated with 10% DA-3711 showed a 2-fold higher proliferation and 2 to 4-fold higher collagen synthesis than untreated cells. DA-3711 also exhibited anti-oxidative effects, since cells under peroxide-induced oxidative stress showed a 30% higher viability in DA-3711-containing medium than in medium without DA-3711 addition. The results suggest that DA-3711 may have anti-aging effects by stimulating skin regeneration and protecting against oxidative stress.

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Effects of 7-MEGATM 500 on Oxidative Stress, Inflammation, and Skin Regeneration in H2O2-Treated Skin Cells

  • Song, In-Bong;Gu, Hyejung;Han, Hye-Ju;Lee, Na-Young;Cha, Ji-Yun;Son, Yeon-Kyong;Kwon, Jungkee
    • Toxicological Research
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    • 제34권2호
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    • pp.103-110
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    • 2018
  • Environmental stimuli can lead to the excessive accumulation of reactive oxygen species (ROS), which is one of the risk factors for premature skin aging. Here, we investigated the protective effects of $7-MEGA^{TM}$ 500 (50% palmitoleic acid, 7-MEGA) against oxidative stress-induced cellular damage and its underlying therapeutic mechanisms in the HaCaT human skin keratinocyte cell line (HaCaT cells). Our results showed that treatment with 7-MEGA prior to hydrogen peroxide ($H_2O_2$)-induced damage significantly increased the viability of HaCaT cells. 7-MEGA effectively attenuated generation of $H_2O_2$-induced reactive oxygen species (ROS), and inhibited $H_2O_2$-induced inflammatory factors, such as prostaglandin $E_2$ ($PGE_2$), tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), and $interleukin-1{\beta}$ ($IL-1{\beta}$). In addition, cells treated with 7-MEGA exhibited significantly decreased expression of matrix metalloproteinase-1 (MMP-1) and increased expression of procollagen type 1 (PCOL1) and Elastin against oxidative stress by $H_2O_2$. Interestingly, these protective activities of 7-MEGA were similar in scope and of a higher magnitude than those seen with 98.5% palmitoleic acid (PA) obtained from Sigma when given at the same concentration (100 nL/mL). According to our data, 7-MEGA is able to protect HaCaT cells from $H_2O_2$-induced damage through inhibiting cellular oxidative stress and inflammation. Moreover, 7-MEGA may affect skin elasticity maintenance and improve skin wrinkles. These findings indicate that 7-MEGA may be useful as a food supplement for skin health.