• Title/Summary/Keyword: tumor necrosis factor-a

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Different level of tumor necrosis factor-α expression after administration of silk sericin fraction in RAW264.7 cells

  • Kim, Dae-Won;Jo, You-Young;Kweon, HaeYong;Kim, Seong-Gon
    • International Journal of Industrial Entomology and Biomaterials
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    • v.41 no.1
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    • pp.1-5
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    • 2020
  • Tumor necrosis factor-α (TNFα) is a representative marker for inflammation. Silk sericin is known as mild TNFα inducer. The purpose of this study was to compare the level of TNFα among different fractions of silk sericin. Silk sericin was extracted from cocoon and separated it by molecular weight. Each fraction was applied to RAW264.7 cells. The level of TNFα was evaluated by western blot and ELISA assay. In results, the level of TNFα was increased as time-dependent manner. Higher molecular weight fraction of sericin induced higher amount of TNFα than lower molecular weight fraction. In conclusion, different molecular weight fraction of sericin induced TNFα differently.

Influence of Autologous and Homologous Blood Transfusion on Interleukins and Tumor Necrosis Factor-α in Peri-operative Patients with Esophageal Cancer

  • Xing, Yue-Li;Wang, Yan-Chun
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.18
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    • pp.7831-7834
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    • 2014
  • Objective: To explore the influence of different ways of blood transfusion on the expression levels of interleukins (IL) and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) inperi-operative patients with esophageal cancer. Materials and Methods: A total of 80 patients with esophageal cancer who underwent radical operations were selected as study patients and randomly divided into an observation group (treated with autologous blood transfusion) and control group (with homologous blood transfusion). Changes of intra-operative indexes and peri-operative blood indexes, from hemoglobin (Hb) and hematocrit value (Hct), to levels of inflammatory factors like interleukins-6 (IL-6), IL-8, IL-10 and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) were compared. Results: Operations for patients in both groups were successfully conducted, and no significant differences in mean surgical duration and intra-operative hemorrhage volume, fluid infusion volume and blood transfusion volume were detected (p>0.05). Compared with values before surgery, Hb and Hct levels decreased significantly while white blood cell count (WBC) increased 1, 5 and 7 d after operation (p<0.05, p<0.01). In addition, WBC was apparently higher in observation group than in control group 5 and 7 d after operation (p<0.01). Compared with before surgery, in the observation group, levels of IL-6, IL-8 and IL-10 had no significant differences after operation (P>0.05), but TNF-${\alpha}$ level increased y (p<0.01), whereas in control group, IL-6 level had no significant difference (p>0.05), IL-8 level decreased obviously (p<0.05), IL-10 level increased markedly first and then decreased gradually as time passed but its level remained elevated (p<0.01), and TNF-${\alpha}$ level increased first and then decreased, and there was no significant difference 7 d after operation (p>0.05). Conclusions: Decreased IL-8 and increased IL-10 levels are two important reasons for immunosuppression after homologous blood transfusion, whereas autologous blood transfusion can alleviate this while increasing the TNF-${\alpha}$ level, which also has potential to improve anti-tumor immunity in the human body.

No Association between Tumor Necrosis Factor-alpha Gene Polymorphisms and Lung Cancer Risk

  • Kim, Jin Hee;Hong, Yun-Chul
    • Environmental Analysis Health and Toxicology
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    • v.28
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    • pp.12.1-12.5
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    • 2013
  • Objectives The role of genetic polymorphisms of tumor necrosis factor-alpha (TNF-${\alpha}$) for lung cancer development was evaluated. Methods Genotypes of the TNF-${\alpha}$ polymorphisms, -1210C>T, -487A>G, -417A>G, IVS1+123G>A, and IVS3+51A>G, were determined in 616 lung cancer cases and 616 lung cancer-free controls. Results After adjusting for body mass index and smoking, each TNF-${\alpha}$ genotype or haplotype composed of five TNF-${\alpha}$ single nucleotide polymorphisms did not show an association with lung cancer risk (p>0.05). The statistical power was found to be 88.4%, 89.3%, 93.3%, 69.7%, and 93.9% for 1210C>T, -487A>G, -417A>G, IVS1+123G>A, and IVS3+51A>G, respectively. Furthermore, the effects of each SNP or haplotype on lung cancer risk were not found to be different according to the cell type of lung cancer (p>0.05). In the repeated analysis with only subjects without other diseases related to inflammation, there was also no association between polymorphisms or haplotypes of the TNF-${\alpha}$ gene and lung cancer risk (p>0.05). Conclusions This study found no association between common variants of the TNF-${\alpha}$ gene and lung cancer risk.

Tumor Necrosis factor-α Promotes Osteogenesis of Human Bone Marrow-derived Mesenchymal Stem Cells through JNK-dependent Pathway (Tumor necrosis factor-α에 의한 골수 유래 중간엽 줄기세포의 골세포로의 분화 촉진에서 JNK의 역할)

  • Kim, Mi-Ra;Song, Hae-Young;Kim, Jae-Ho
    • Journal of Life Science
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    • v.16 no.7 s.80
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    • pp.1207-1213
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    • 2006
  • Tumor necrosis $factor-{\alpha}\;(TNF-{\alpha})$ has been implicated in skeletal diseases by promoting bone loss in inflammatory bone diseases. In the present study, we examined the effects of $TNF-{\alpha}$ on osteoblastic differentiation of human bone marrow-derived mesenchymal stem cells (hBMSCs). $TNF-{\alpha}$ dose-dependently promoted matrix mineralization of hBMSCs with a maximal stimulation at 2ng/ml. $TNF-{\alpha}$ increased expression of alkaline phosphatase, which plays a crucial role for the matrix deposition. The $TNF-{\alpha}-stimulated$ osteoblastic differentiation was not affected by $NF_kB$ inhibitors, BAY and SN50. However, a JNK-specific inhibitor, SP600125 completely abolished the $TNF-{\alpha}-stimulated$ matrix mineralization and expression of alkaline phosphatase. These results suggest that $TNF-{\alpha}$ enhances osteoblastic differentiation of hBMSCs through JNK-dependent pathway.

Sequential changes of Interleukin-6, Tumor Necrosis Factor-$\alpha$, and Troponin-T During Open Heart Surgery with Cardiopulmonary Bypass (체외순환을 이용한 심장수술시 혈청 Interleukin-6, Tumor Necrosis Factor-$\alpha$와 Troponin-T의 시간대별 변화)

  • 류지윤;최석철;곽기오;최국렬;김송명;조광현
    • Journal of Chest Surgery
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    • v.32 no.11
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    • pp.971-977
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    • 1999
  • Background: Immunologic and inflammatory responses of cardiopulmonary bypass(CPB) influence postoperative mortality and morbidity with multiple organ injury. It has been reported that ischemia/reperfusion induced-myocardial injury during CPB is causative of release of inflammatory cytokines such as interleukin-6(IL-6) and tumor necrosis factor-$\alpha$ (TNF-$\alpha$). The purpose of this study was to detect the time course of the activated cytokine and troponin-T(TnT), and to examine the correlation between such parameters during CPB. Material and Method: The serial samples were collected from arterial blood via radial arterial catheter in 23 patients who are underwent open heart surgery (OHS) with CPB, the IL-6, TNF-$\alpha$ and TnT were checked. Result: \circled1 IL-6, TNF$\alpha$- and TnT concentration increased significantly during CPB with a peaking level of CPB-off (p 0.05). \circled2 IL-6 had highly positive correlation with aortic cross clamping time and total bypass time(r=0.80, 0.78; p 0.05, respectively). \circled3 There was no correlation among IL-6, TNF-$\alpha$ and TnT. Conclusion: In conclusion, these data showed that elevated production of serum IL-6 during CPB was attributable to ischemia/reperfusion induced-myocardial damage. IL-6 will become a new and sensitive biological marker in assessment of myocardial damage during OHS with CPB. However, further studies will be needed to apply IL-6 in more patient population.

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Cell Surface Expression of Tumor Necrosis Factor-Alpha by Activated Rat Astrocytes

  • Chung, Il-Yup;Benveniste, Etty N.
    • BMB Reports
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    • v.29 no.6
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    • pp.530-534
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    • 1996
  • Astrocyte are the major glial cell type in the central nervous system (CNS), and analogous to macrophage, mediates the number of immune responses such as production of cytokines including tumor necrosis factor alpha ($TNF-{\alpha}$) upon activation. $TNF-{\alpha}$ has been implicated in neuroimmunological disorders through killing oligodendrocytes and thus causing demyelination. It has been previously demonstrated that mitogen-activated T cells synthesized a 26 kDa precursor form of $TNF-{\alpha}$ which is bound to the surface of a membrane, and is later secreted as a 17 kDa mature version. In order to examine whether astrocytes would produce the transmembrane form of $TNF-{\alpha}$, astrocytes were stimulated with biological stimuli and the membrane form of $TNF-{\alpha}$ was analyzed by Western blot and FACS analysis. When astrocytes are stimulated with lipopolysaccharide (LPS), $IFN-{\gamma}/LPS$, or $IFN-{\gamma}/IL-1{\beta}$, they were able to express a membrane-anchored $TNF-{\alpha}$ of approximately 26 kDa protein which was immunoreactive to an $anti-TNF-{\alpha}$ antibody, whereas unstimulated astrocytes or astrocytes treated with $IFN-{\gamma}$ or $IL-1{\beta}$ alone was not. Our FACS data were also consistent with the immunoblot analysis. Our result suggests that the membrane form of $TNF-{\alpha}$ expressed by activated astrocytes may cause local damage to oligodendrocytes by direct cell-cell contact and contribute to demyelination observed in multiple sclerosis (MS) and experimental allergic encephalomyelitis (EAE).

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Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Activates Pro-Survival Signaling Pathways, Nuclear Factor-${\kappa}B$ and Extracellular Signal-Regulated Kinase 1/2 in Trophoblast Cell Line, JEG-3

  • Ka Hakhyun
    • Reproductive and Developmental Biology
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    • v.29 no.2
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    • pp.101-108
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    • 2005
  • Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) is a well-known inducer of apoptotic cell death in many tumor cells. 1RAIL is expressed in human placenta, and cytotrophoblast cells express 1RAIL receptors. However, the role of TRAIL in human placentas and cytotrophoblast cells is not. well understood. In this study a trophoblast cell line, JEG-3, was used as a model system to examine the effect of TRAIL. on key intracellular signaling pathways involved in the control of trophoblastic cell apoptosis and survival JEG-3 cells expressed receptors for 1RAIL, death receptor (DR) 4, DR5, decoy receptor (OcR) 1 and DeR2. Recombinant human TRAIL (rhTRAIL) did not have a cytotoxic effect determined by MIT assay and did not induce apoptotic cell death determined by poly-(ADP-ribose) polymerase cleavage assay. rhTRAIL induced a rapid and transient nuclear translocation of nuclear $factor-{\kappa}B(NF-{\kappa}B)$ determined by immunoblotting using nuclear protein extracts. rhTRAIL rapidly activated extracellular signal-regulated protein kinase (ERK) 1/2 as determined by immnoblotting for phospho-ERK1/2. However, c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (p38MAPK) and Akt (protein kinase B) were not activated by rhTRAIL. The ability of 1RAIL to induce $NF-{\kappa}B$ and ERK1/2 suggests that interaction between TRAIL and its receptors may play an important role in trophoblast cell function during pregnancy.

Rubus croceacanthus Leveille inhibits mast cell-mediated immediate-type allergic reactions and tumor necrosis factor-$\alpha$ secretion

  • Moon, Phil-Dong;Park, In-Young;Na, Ho-Jeong;Hong, Seung-Heon;Kim, Hyung-Min
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 2003.11a
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    • pp.99-99
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    • 2003
  • We studied the effect of Rubus croceacanthus Leveille (RCL) on mast cell-mediated anaphylactic reactions. RCL inhibited compound 48/80-induced systemic anaphylactic shock. When RCL was given at concentrations ranging from 0.01 to 1 mg/$m\ell$, the histamine release from rat peritoneal mast cells induced by compound 48/80 was reduced in a dose-dependent manner. RCL also inhibited passive cutaneous anaphylaxis activated by anti-dinitrophenyl IgE. In addition, RCL inhibited phorbol 12-myristate 13-acetate and A23187-induced tumor necrosis factor-${\alpha}$ secretion from human mast cell line HMC-1 cells. These results indicate that RCL may possess a strong anti-anaphylactic activity.

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Effect of Unripened fruits and Ripened fruits of Rubus coreanus Miquel on Murine Peritoneal Macrophages (복분자 미숙과 및 성숙과가 생쥐의 복강 Macrophages에 미치는 영향)

  • Lee Taek Yul;Kim Dae Keun;So June No;Kwon Jin;Song Jung Mo;Eun Jae Soon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.17 no.4
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    • pp.991-995
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    • 2003
  • The purpose of this research was to investigate the effects of unripened fruits and ripened fruits of Rubus coreanus Miquel on murine peritoneal macrophages. The 70% ethyl alcohol extracts (20 or 100 mg/kg) of unripened fruits (RCE-I) and of ripened fruits (RCE-II) were administered p.o. once a day for 7 days to mice. RCE-I and RCE-II decreased the phagocytic activity of murine peritoneal macrophages and the production of nitric oxide. Also, RCE-I and RCE-II increased the production of tumor necrosis factor- a from peritoneal macrophages. In general, the immuno-suppressive action of RCE-I on macrophages was more potent than those of RCE-II. These results suggest that the fruits of Rubus coreanus Miquel regulates the non-specific immune response via decrease of phagocytic activity and increase of production of tumor necrosis factor- a from murine peritoneal macrophages.

Expression of Tumor Necrosis Factor-alpha-induced Protein 8 in Pancreas Tissues and its Correlation with Epithelial Growth Factor Receptor Levels

  • Liu, Ke;Qin, Cheng-Kun;Wang, Zhi-Yi;Liu, Su-Xia;Cui, Xian-Ping;Zhang, Dong-Yuan
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.3
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    • pp.847-850
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    • 2012
  • Tumor necrosis factor (TNF)-alpha-induced protein 8 (TNFAIP8 or TIPE) is a recently identified protein considered to be associated with carcinogenesis. To investigate its expression pattern in pancreatic cancer patients and to analyse its correlation with clinicopathological significance and the expression levels of epithelial growth factor receptor (EGFR), immunohistochemistry was performed to detect the TNFAIP8 and EGFR proteins in pancreatic cancers, pancreatitis tissues, and healthy controls. The results showed stronger staining of TNFAIP8 protein in pancreatic cancer tissues compared with normal pancreas tissue. Furthermore, in 56 patients with pancreatic cancer, the expression levels of TNFAIP8 in patients with low tumor stage was higher than that with high tumor stage, and correlated with tumor staging and lymph node metastasis (P<0.05). Furthermore, TNFAIP8 expression positively correlated with EGFR levels (r=0.671135, P<0.05). These results indicate that TNFAIP8 may play important roles in the progression of pancreatic cancer.