• Title/Summary/Keyword: p53 activation

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Resveratrol Inhibits Nitric Oxide-Induced Apoptosis via the NF-Kappa B Pathway in Rabbit Articular Chondrocytes

  • Eo, Seong-Hui;Cho, Hongsik;Kim, Song-Ja
    • Biomolecules & Therapeutics
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    • v.21 no.5
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    • pp.364-370
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    • 2013
  • Resveratrol (trans-3,4'-trihydroxystillbene), a naturally occurring polyphenolic antioxidant found in grapes and red wine, elicits diverse biochemical responses and demonstrates anti-aging, anti-inflammatory, and anti-proliferative effects in several cell types. Previously, resveratrol was shown to regulate differentiation and inflammation in rabbit articular chondrocytes, while the direct production of nitric oxide (NO) in these cells by treatment with the NO donor sodium nitroprusside (SNP) led to apoptosis. In this study, the effect of resveratrol on NO-induced apoptosis in rabbit articular chondrocytes was investigated. Resveratrol dramatically reduced NO-induced apoptosis in chondrocytes, as determined by phase-contrast microscopy, the MTT assay, FACS analysis, and DAPI staining. Treatment with resveratrol inhibited the SNP-induced expression of p53 and p21 and reduced the expression of procaspase-3 in chondrocytes, as detected by western blot analysis. SNP-induced degradation of I-kappa B alpha ($I{\kappa}B-{\alpha}$) was rescued by resveratrol treatment, and the SN50 peptide-mediated inhibition of NF-kappa B (NF-${\kappa}B$) activity potently blocked SNP-induced caspase-3 activation and apoptosis. Our results suggest that resveratrol inhibits NO-induced apoptosis through the NF-${\kappa}B$ pathway in articular chondrocytes.

Preparation and characterization of green adsorbent from waste glass and its application for the removal of heavy metals from well water

  • Rashed, M. Nageeb;Gad, A.A.;AbdEldaiem, A.M.
    • Advances in environmental research
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    • v.7 no.1
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    • pp.53-71
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    • 2018
  • Waste glass disposal causes environmental problems in the cities. To find a suitable green environmental solution for this problem low cost adsorbent in this study was prepared from waste glass. An effective new green adsorbent was synthesized by hydrothermal treatment of waste glass (WG), followed by acidic activation of its surface by HCl (WGP). The prepared adsorbent was characterized by scanning electron microscopy (SEM), X-ray fluorescence (XRF), X-ray diffraction (XRD), and BET surface measurement. The developed adsorbent was used for the removal of heavy metals (Cd, Cu, Fe, Pb and Zn) from well water. Batch experiments were conducted to test the ability of the prepared adsorbent for the removal of Cd, Cu, Fe, Pb and Zn from well water. The experiments of the heavy metals adsorption by adsorbent (WGP) were performed at different metal ion concentrations, solution pH, adsorbent dosage and contact time. The Langmuir and Freundlich adsorption isotherms and kinetic models were used to verify the adsorption performance. The results indicated high removal efficiencies (99-100%) for all the studied heavy metals at pH 7 at constant contact time of 2 h. The data obtained from adsorption isotherms of metal ions at different time fitted well to linear form of the Langmuir sorption equation, and pseudo-second-order kinetic model. Application of the resulted conditions on well water demonstrated that the modified waste glass adsorbent successfully adsorbed heavy metals (Cd, Cu, Fe, Pb and Zn) from well water.

Induction of Apoptosis by Yukwool-tang in Human Cervical Carcinoma HeLa Cells (육울탕(六鬱湯)에 의한 인체자궁경부암세포의 증식억제에 관한 연구)

  • Choi, Yung-Hyun;Choi, Byung-Tae;Lee, Yong-Tae
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.21 no.6
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    • pp.1513-1519
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    • 2007
  • Yukwool-tang (YWT) is a traditional Chinese medicine, which has been used for patients suffering from a uterine disease in Oriental medicine. In the present study, it was examined the biochemical mechanisms of apoptosis by YWT in human cervical carcinoma HeLa cells. It was found that YWT could inhibit the cell growth of HeLa cells in a dose-dependent manner, which was associated with apoptotic cell death such as formation of apoptotic bodies and DNA fragmentation. Flow cytometry analysis confirmed that YWT treatment increased populations of apoptotic-sub-G1 phase of the cell cycle. We observed the p53-independent induction of p21 proteins, down-regulation of anti apoptotic Bcl-2 expression and proteolytic activation of caspase-3 in YWT-treated HeLa cells. YWT treatment also concomitant degradation and/or inhibition of poly (ADP-ribose) polymerase (PARP), phospholipase C-1 ($PLC{\gamma}1$), ${\beta}-catenin$ and DNA fragmentation factor 45/inhibitor of caspase-activated DNase (DFF45/ICAD). Taken together, these findings partially provide novel insights into the possible molecular mechanism of the anti-cancer activity of YWT.

Chemical Composition and Rheological Properties of Polysaccharides Isolated from Different Parts of Brown Seaweed Undaria pinnatifida (미역(Undaria pinnatifida) 부위별로 추출한 다당의 이화학적 특성)

  • Koo, Jae-Geun
    • Korean Journal of Fisheries and Aquatic Sciences
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    • v.53 no.5
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    • pp.665-671
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    • 2020
  • The chemical and rheological properties of fucoidan and alginate prepared from different parts of Undaria pinnatifida (sporophyll, frond, stipe) were investigated. The algal materials were extracted with HCl (pH 2.0, 3 h at 70℃) to prepare fucoidan, and the remaining solid was continuously re-extracted with Na2CO3 (pH 10.0, 70℃, 3 h) to prepare alginic acid. The fucoidan and alginic acid contents in the sporophyll, frond, and stipe were 11.14%, 3.84%, and 1.73% and 22.04%, 37.14%, and 31.74%, respectively. The content of fucoidan and alginate depends on the part extracted. The fucoidan extracted from the sporophyll mainly consists of fucose and galactose, but the fucoidan extracted from frond and stipe contains mannose in addition to fucose and galactose. Fourier-transform infrared spectroscopy analysis of fucoidan and alginate suggests the presence of sulfate groups (1261 and 840 cm-1) and carboxyl groups (1626 and 1419 cm-1), respectively. Alginate solutions (5%) had a low viscosity of 10.84-31.63 mPa·s. The activation energies of fucoidan and sodium alginate were 14.45-18.38 kJ/mol and 18.61-22.06 kJ/mol, respectively. The D-mannuronic acid/L-guluronic acid (M/G) ratios of alginate showed a relatively high (frond, 3.72; stipe, 2.88; and sporophyll, 1.80).

A Characteristics of Environmental Fraternitive Photopolymerization and Thermal Degradation on Methyl Methacrylate (메틸메타크릴레이트의 환경친화적인 광중합 및 열분해특성)

  • 주영배;이내우;최재욱;강돈오;설수덕
    • Journal of the Korean Society of Safety
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    • v.16 no.3
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    • pp.68-75
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    • 2001
  • Photopolymerization, the utilization of electromagnetic radiation(or light) as the energy source for polymerization of functional monomers, oligomers is the basis of important commercial processes with broad applicability, including photoimaging and RV curing of coatings and inks. The objective of this study is to investigate the characteristics of environmental fraternitive photopolymerization of methyl methacrylate(MMA). This work is the first step to continue further research about alkyl methacrylate. The experiment was done in aqueous solution under the influence of photo-initiator concentration(0.05-0.25mol/l), light intensity (5000-9000 ${\mu}J/cm^2$) and monomer concentration(2-6mol/l). Methyl methacrylate was polymerized to high conversion ratio using hydrogen peroxide($H_2O_2$) and the kinetics model we have obtained is as follows. $R_p=k_p[S]^{0.41}[M]^{0.62}[L]^{2.45} exp(53.64/RT$). The differential method of thermogravimetric analysis(Friedman method) was used to obtain value of activation energy on decomposition reaction. The average value of it res 45.4Kca1/mol.

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A77 1726 Inhibit NO-induced Apoptosis via PI-3K/AKT Signaling Pathway in Rabbit Articular Chondrocyte

  • Choi, In-Kyou;Kim, Song-Ja
    • Biomedical Science Letters
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    • v.15 no.1
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    • pp.61-66
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    • 2009
  • Leflunomide is an immunomodulatory agent used for the treatment of rheumatoid arthritis (RA). Leflunomide known as a regulator of iNOS synthesis which largely decreases NO production in diverse cell type. However, the effect of leflunomide on chondrocyte is still poorly understood. In our previous studies, we have shown that direct production of Nitric oxide (NO) by treating chondrocytes with NO donor, sodium nitroprusside (SNP), causes apoptosis via p38 mitogen-activated protein kinase in association with elevation of p53 protein level, caspase-3 activation. In this study, we characterized the molecular mechanism by which A77 1726 inhibit apoptosis. We found that A77 1726 inhibit NO-induced apoptosis as determined by MTT (Thiazolyl Blue Tetrazolium Bromide) assay and DNA fragmentation. The inhibition of apoptosis by A77 1726 was accompanied by increased PI-3 kinase and AKT activities. So, inhibition of phosphatidylinositol (PI)-3kinase with LY294002 rescued apoptosis. Triciribine, the specific inhibitor of AKT, also abolished anti-apoptotic effect. Our results indicate that A77 1726, the active metabolite of leflunomide, mediates NO-induced apoptosis in chondrocytes by modulating up-regulation of PI-3 kinase and AKT.

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Structural characterization of As-MIF and hJAB1 during the inhibition of cell-cycle regulation

  • Park, Young-Hoon;Jeong, Suk;Ha, Ki-Tae;Yu, Hak Sun;Jang, Se Bok
    • BMB Reports
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    • v.50 no.5
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    • pp.269-274
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    • 2017
  • The biological activities of macrophage migration inhibitory factor (MIF) might be mediated through a classical receptor-mediated or non-classical endocytic pathway. JAB1 (C-Jun activation domain-binding protein-1) promotes the degradation of the tumor suppressor, p53, and the cyclin-dependent kinase inhibitor, p27. When MIF and JAB1 are bound to each other in various intracellular sites, MIF inhibits the positive regulatory effects of JAB1 on the activity of AP-1. The intestinal parasite, Anisakis simplex, has an immunomodulatory effect. The molecular mechanism of action of As-MIF and human JAB1 are poorly understood. In this study, As-MIF and hJAB1 were expressed and purified with high solubility. The structure of As-MIF and hJAB1 interaction was modeled by homology modeling based on the structure of Ace-MIF. This study provides evidence indicating that the MIF domain of As-MIF interacts directly with the MPN domain of hJAB1, and four structure-based mutants of As-MIF and hJAB1 disrupt the As-MIF-hJAB1 interaction.

The Effects of Jawoongo(紫雲膏) on UVB Damage to Skin And Photoaging (자운고(紫雲膏)가 자외선에 의한 피부손상 및 광노화(光老化)에 미치는 영향)

  • Jeon, Jae-Hong;Hong, Seung-Ug
    • The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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    • v.20 no.1 s.32
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    • pp.130-144
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    • 2007
  • UV-irradiated skin shows acutely erythema, edema, pigmantation (sunbum) and chronically coarse wrinkling, roughness, dryness, laxity (photoaging). Jawoongo(紫雲膏, JW) is clinically useful external application and effective bum, sunburn, wound and symptom of dryness(燥症) in skin disease. In this experiment, we examined if JW could cure the UVB-mediated acute skin damages, inhibit UVB-mediated oxidative stress and inflammation of skin, and block the photoaging. In vivo test, we found that JW could effectively cure the UVB-mediated acute skin damages(erythema, edema, angiogenesis, hyperplasia, infiltration of lymphocytes) and inhibit expression of HSP70, CYP1A1 and p53. We also found that JW could repair destruction of collagen fiber and inhibit activation of MMP-9, and inhibit expression of $NF-{\kappa}B$ p65, iNOS, hyperplasia of keratynocyte. In vitro test, we found that JW could inhibit expression of IKK, iNOS mRNA, and production of NO. These findings shows that JW could cure the UVB-mediated acute skin damages, inhibit UVB-mediated oxidative stress and inflammation of skin, and block photoaging.

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Characterization of arsenic doped p-type ZnO thin film (As 토핑된 p형 ZnO 박막의 특성 분석)

  • Kim, Dong-Lim;Kim, Gun-Hee;Chang, Hyun-Woo;Ahn, Byung-Du;Lee, Sang-Yeol
    • Proceedings of the KIEE Conference
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    • 2006.10a
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    • pp.53-54
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    • 2006
  • Arsenic doped p-type ZnO thin films have been realized on intrinsic (100) GaAs substrate by RF magnetron sputtering and thermal annealing treatment. p-Type ZnO exhibits the hole concentration of $9.684{\times}10^{19}cm^3$, resistivity of $2.54{\times}10^{-3}{\Omega}cm$, and mobility of $25.37\;cm^2/Vs$. Photoluminescence (PL) spectra of As doped p-type ZnO thin films reveal neutral acceptor bound exciton ($A^{0}X$) of 3.3437 eV and a transition between free electrons and acceptor levels (FA) of 3.2924 eV. Calculated acceptor binding energy ($E_A$) is about 0.1455 eV. Thermal activation and doping mechanism of this film have been suggested by using X-ray photoelectron spectroscopy (XPS). p-Type formation mechanism of As doped ZnO thin film is more related to the complex model, namely, $As_{Zn}-2V_{Zn}$, in which the As substitutes on the Zn site, rather than simple model, Aso, in which the As substitutes on the O site. ZnO-based p-n junction was fabricated by the deposition of an undoped n-type ZnO layer on an As doped p-type ZnO layer.

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ACOX1 destabilizes p73 to suppress intrinsic apoptosis pathway and regulates sensitivity to doxorubicin in lymphoma cells

  • Zheng, Fei-Meng;Chen, Wang-Bing;Qin, Tao;Lv, Li-Na;Feng, Bi;Lu, Yan-Ling;Li, Zuo-Quan;Wang, Xiao-Chao;Tao, Li-Ju;Li, Hong-Wen;Li, Shu-You
    • BMB Reports
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    • v.52 no.9
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    • pp.566-571
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    • 2019
  • Lymphoma is one of the most curable types of cancer. However, drug resistance is the main challenge faced in lymphoma treatment. Peroxisomal acyl-CoA oxidase 1 (ACOX1) is the rate-limiting enzyme in fatty acid ${\beta}$-oxidation. Deregulation of ACOX1 has been linked to peroxisomal disorders and carcinogenesis in the liver. Currently, there is no information about the function of ACOX1 in lymphoma. In this study, we found that upregulation of ACOX1 promoted proliferation in lymphoma cells, while downregulation of ACOX1 inhibited proliferation and induced apoptosis. Additionally, overexpression of ACOX1 increased resistance to doxorubicin, while suppression of ACOX1 expression markedly potentiated doxorubicin-induced apoptosis. Interestingly, downregulation of ACOX1 promoted mitochondrial location of Bad, reduced mitochondrial membrane potential and provoked apoptosis by activating caspase-9 and caspase-3 related apoptotic pathway. Overexpression of ACOX1 alleviated doxorubicin-induced activation of caspase-9 and caspase-3 and decrease of mitochondrial membrane potential. Importantly, downregulation of ACOX1 increased p73, but not p53, expression. p73 expression was critical for apoptosis induction induced by ACOX1 downregulation. Also, overexpression of ACOX1 significantly reduced stability of p73 protein thereby reducing p73 expression. Thus, our study indicated that suppression of ACOX1 could be a novel and effective approach for treatment of lymphoma.