• Title/Summary/Keyword: factor-{\alpha}$

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Hypoxia-inducible Factor 1 Alpha (HIF-1α) as a Prognostic Indicator in Patients with Gastric Tumors: A Meta-analysis

  • Zhang, Zhi-Gang;Zhang, Qiu-Ning;Wang, Xiao-Hu;Tian, Jin-Hui
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.7
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    • pp.4195-4198
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    • 2013
  • Background and Objective: Though researched for years, the prognostic role of hypoxia-inducible factor 1 alpha (HIF-$1{\alpha}$) in gastric cancer is still controversial. We thus undertook a systematic review to assess the relationship. Method: A systematically literature search of Pubmed, Embase, Web of Science, China Biological Medicine Disc and Cochrane Library was undertaken in February 2013, and the reference lists of articles were retrieved. Results: 12 trials (1,555 participants) were included to assess the association between HIF-$1{\alpha}$ expression and survival. Summary hazard ratios (HRs) were calculated. HIF-$1{\alpha}$ expression was significantly correlated with poor overall survival of gastric cancer patients (HR=1.34, 95%CI: 1.13-1.58; P=0.0009), but not with poor disease free survival of gastric cancer patients (HR=1.67, 95%CI: 0.99-2.82; P=0.06). Conclusion: HIF-$1{\alpha}$ was associated with poor OS, but not DFS, especially for Asian patients. But studies evaluating relationships of HIF-$1{\alpha}$ with OS and DFS in non-Asian gastric cancer patients appear needed.

Anti-inflammatory Effect of Angelicae acutilobae Radix Water Extract on LPS-stimulated Mouse Macrophages (마우스 대식세포를 이용한 일당귀 물추출물의 항염효능 연구)

  • Han, Hyo-Sang
    • The Korea Journal of Herbology
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    • v.28 no.6
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    • pp.129-133
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    • 2013
  • Objectives : The purpose of this study was to investigate the effects of Angelicae acutilobae Radix Water Extract (AA) on the production of cytokines in RAW 264.7 cell stimulated with lipopolysaccharide (LPS). Method : RAW 264.7 cells were cotreated with AA (50 and $100{\mu}g/mL$) and lipopolysaccharide (LPS; $1{\mu}g/mL$) for 24 hours. After 24 hours treatment, using bead-based multiplex cytokine assay, concentrations of various cytokines such as interleukin(IL)-6, tumor necrosis factor-alpha(TNF-${\alpha}$) granulocyte colony-stimulating factor(G-CSF), granulocyte macrophage colony-stimulating factor(GM-CSF), and macrophage inflammatory protein(MIP)-$1{\alpha}$ were measured. Result : AA significantly inhibited LPS-induced production of IL-6 and MIP-$1{\alpha}$ from LPS-stimulated RAW 264.7 cells at the concentration of $50{\mu}g/mL$. AA significantly inhibited LPS-induced production of TNF-${\alpha}$ from LPS-stimulated RAW 264.7 cells at the concentration of $100{\mu}g/mL$. AA significantly inhibited LPS-induced production of G-CSF and GM-CSF in RAW 264.7 cells at the concentrations of 50 and $100{\mu}g/mL$. Conclusion : These results suggest that AA has anti-inflammatory effect related with its inhibition of proinflammatory cytokines such as IL-6, TNF-${\alpha}$, G-CSF, GM-CSF, and MIP-$1{\alpha}$ in LPS-induced macrophages.

Effect of Conjugated Linoleic Acid on Nuclear Factor-${\kappa}B$ Activation and Tumor Necrosis Factor-${\alpha}$ Production in RAW 264.7 Cells Exposed to High Concentration of Glucose (고농도의 당에 노출된 RAW 264.7 세포에서 conjugated linoleic acid의 TNF-${\alpha}$ 생산과 NF-${\kappa}B$의 활성 효과)

  • Lee, Minji;Kang, Byeong-Teck;Kang, Ji-Houn;Yang, Mhan-Pyo
    • Journal of Veterinary Clinics
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    • v.29 no.5
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    • pp.361-367
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    • 2012
  • Diabetes-related complications in human and veterinary medicine have been shown to be associated with hyperglycemia-induced inflammation. It has been recently suggested that the onset of insulin resistance may be caused by over-production of inflammatory cytokines such as tumor necrosis factor (TNF)-${\alpha}$ from immune cells. Conjugated linoleic acid (CLA) regulates inflammatory response through modulation of TNF-${\alpha}$ expression. The objective of this study was to examine the effect of CLA on nuclear factor kappaB (NF-${\kappa}B$) p65 binding activity, inhibitory kappaB ($I{\kappa}B$)-${\alpha}$ expression, and TNF-${\alpha}$ production from high glucose-treated RAW 264.7 cells. CLA was added to RAW cells that had been previously cultured with low or high concentration of glucose. The levels of TNF-${\alpha}$ protein in the culture supernatant of RAW cells exposed to high concentrations of glucose were higher than those of cells exposed to low concentrations of glucose. The treatment with the high concentration of glucose in RAW cells increased levels of NF-${\kappa}B$ p65 binding activity and the decreased $I{\kappa}B-{\alpha}$ expression when compared with those of low glucose. The treatments in combination with CLA and glucose (low and high) glucose in RAW cells increased TNF-${\alpha}$ production when compared with that glucose alone. These treatments with CLA increased TNF-${\alpha}$ production in high glucose-treated RAW cells than those with low glucose. These treatments of CLA also showed higher NF-${\kappa}B$ p65 binding activity and lower $I{\kappa}B-{\alpha}$ expression in high glucose than those in low glucose condition. This suggests that CLA can increase NF-${\kappa}B$ p65 binding activity and TNF-${\alpha}$ production from high glucose-treated RAW 264.7 cells and is likely to promote hyperglycemia-induced inflammation.

Induction of Heat Shock Protein 70 Inhibits Tumor Necrosis $Factor{\alpha}-induced$ Lipid Peroxidation in Rat Mesangial Cells (Heat Shock Protein 70이 흰쥐 배양 혈관간 세포에서 관찰되는 $TNF{\alpha}$에 의한 지질과산화에 미치는 보호 효과)

  • Ha, Hun-Joo;Park, Young-Mee;Ahn, Young-Soo;Kim, Kyung-Hwan
    • The Korean Journal of Pharmacology
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    • v.31 no.3
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    • pp.323-331
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    • 1995
  • Monocyte/macrophage infiltration is the well known initial features associated with the development of glomerular disease including non-immune mediated nephropathy. Tumor necrosis factor ${\alpha}(TNF{\alpha})$, a cytokine produced primarily by monocyte/macrophage, exhibits similar effects as observed at the initial stages and during the progression of glomerular injury. Because the mesangial cells are target cells for glomerular injury, the present study examined the effect of $TNF{\alpha}$ on glomerular mesangial cell membrane lipid peroxidation as an index of cytotoxicity attributing to $TNF{\alpha}$. Primary culture of rat mesangial cell was established by incubation of glomeruli isolated from male Sprague-Dawley rat kidneys utilizing a standard sieving method. The levels of lipid peroxides in the mesangial cells were quantitated by malondialdehyde- thiobarbituric acid adduct formation. During an 8 hour incubation at $37^{\circ}C$, $TNF{\alpha}$ at 10 to 10,000 units/ml increased the levels of lipid peroxides dose dependently. Western blot analysis demonstrated that a short thermal stress induced heat shock response and the synthesis of heat shock protein 70(hsp70) in this mesangial cells. Further, this induction of hsp 70 prevented increase of lipid peroxides in the mesangial cells exposed to $TNF{\alpha}$. These data suggest that $TNF{\alpha}-induced$ lipid peroxidation in the mesangial cells may have pathophysiological relevance to glomerular injury and prior induction of heat shock response may play a role in the cellular resistance against $TNF{\alpha}-induced$ glomerular injury.

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Variations of the Linewidth Enhancement Factor of Strained MQW DFB Laser with Output Power (Strained MQW DFB 레이저의 광출력에 따른 Linewidth Enhancement Factor의 변화)

  • 오윤경;곽계달
    • Journal of the Korean Institute of Telematics and Electronics D
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    • v.35D no.6
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    • pp.15-20
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    • 1998
  • The linewidth enhancement factor $\alpha$ and fiber dispersion of 1.55 ${\mu}{\textrm}{m}$ strained multi-quantum well laser diodes are measured using small signal power modulation transfer function in a dispersive fiber. The measured fiber dispersion values are between 16.766 and 16.786ps/nm/km and these are the expected values from standard single mode fiber. To measure the $\alpha$ parameter in the actual operational range of the laser diodes, the dependence of $\alpha$ on laser output power is measured. The $\alpha$ parameter increases linearly as the power of the laser diode increases. This result can explain the non-linear gain effect on the $\alpha$ parameter more accurately than any other measurements.

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Anti-angiogenic Effect of Cryptotanshinone through Inhibition of HIF-1alpha and STAT3 in Prostate Cancer Cells (단삼 유래 단일 물질 cryptotanshione의 전립선 암주에서의 HIF-1alpha와 STAT3 억제를 통한 신생혈관억제효과)

  • Lee, Hyo-Jeong;Hong, Sang-Hyuk;Kim, Sung-Hoon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.26 no.4
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    • pp.437-440
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    • 2012
  • Signal transducer and activator of transcription 3 (STAT3) is a transcription factor that regulates various cellular processes such as cell survival, angiogenesis and proliferation. In the present study, we examined that Cryptotanshione(CT), a tanshinone from oriental traditional medicinal herb Danshen (Salvia miltiorrhiza Bunge), had the inhibitory effects on hypoxia-mediated activation of STAT3 in androgen independent human prostate cancer PC-3 cells. CT inhibited the protein expression of hypoxia-inducible factor-1alpha (HIF-$1{\alpha}$) under hypoxic condition. Consistently, CT blocked hypoxia-induced phosphorylation and nuclear accumulation of STAT3. In addition, CT reduced cellular of vascular endothelial growth factor (VEGF), a critical angiogenic factor and a target gene of STAT3 induced under hypoxia. Of note, chromatin immunoprecipitation (ChiP) assay revealed that CT inhibited binding of STAT3 to VEGF promoter. Taken together, our results suggest that CT has anti-angiogenic activity by disturbing the binding STAT3 to the VEGF promoter in PC-3 cells.

Scutellaria baicalensis ethanol extracts inhibit IGF-II-induced HIF-1 ${\alpha}$ and VEGF expressions in HaCaT cells. (황금 에탄올 추출물이 IGF-II로 유도된 $HIF-1{\alpha}$와 VEGE 발현 억제에 미치는 영향)

  • Byun, Hak-Sung;Kim, Kyung-Jun
    • 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.27-37
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    • 2007
  • Background and Objective : Psoriasis is a chronic skin disease characterized by angiogenesis. It has been reported that growth factor as vascular endothelial growth factor (VEGF) and insulin-like growth factor (IGF)-II are overexpressed in psoriatic epidermis. This stydy was carried out for whether SB extracts have an anti-angiogenic effect for angiogenic factor. Method : To investigate the inhibitory effect of VEGF expression by the SB extracts, we performed MTS assay, western blots using HaCaT cells. HaCaT cells were pretreated with SB extracts for 1 hour followed by treatment with IGF-II. Result : SB extracts significantly reduced IGF-II induced HIF-1 ${\alpha}$ protein level via p53 and MAPK pathway in HaCaT cells. Also, SB extracts inhibited IGF-II induced VEGF mRNA and protein expression levels in the HaCaT keratinocytes. Conclusion : These results suggest that inhibition of HIF-1 ${\alpha}$ and VEGF expressions by SB extracts contributes to the anti-angiogenic effects.

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Apigenin Inhibits Tumor Necrosis Factor-α-Induced Production and Gene Expression of Mucin through Regulating Nuclear Factor-Kappa B Signaling Pathway in Airway Epithelial Cells

  • Seo, Hyo-Seok;Sikder, Mohamed Asaduzzaman;Lee, Hyun Jae;Ryu, Jiho;Lee, Choong Jae
    • Biomolecules & Therapeutics
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    • v.22 no.6
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    • pp.525-531
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    • 2014
  • In the present study, we investigated whether apigenin significantly affects tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-induced production and gene expression of MUC5AC mucin in airway epithelial cells. Confluent NCI-H292 cells were pretreated with apigenin for 30 min and then stimulated with TNF-${\alpha}$ for 24 h or the indicated periods. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription - polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Apigenin significantly inhibited MUC5AC mucin production and down-regulated MUC5AC gene expression induced by TNF-${\alpha}$ in NCI-H292 cells. To elucidate the action mechanism of apigenin, effect of apigenin on TNF-${\alpha}$-induced nuclear factor kappa B (NF-${\kappa}B$) signaling pathway was also investigated by western blot analysis. Apigenin inhibited NF-${\kappa}B$ activation induced by TNF-${\alpha}$. Inhibition of inhibitory kappa B kinase (IKK) by apigenin led to the suppression of inhibitory kappa B alpha ($I{\kappa}B{\alpha}$) phosphorylation and degradation, p65 nuclear translocation. This, in turn, led to the down-regulation of MUC5AC protein production in NCI-H292 cells. Apigenin also has an influence on upstream signaling of IKK because it inhibited the expression of adaptor protein, receptor interacting protein 1 (RIP1). These results suggest that apigenin can regulate the production and gene expression of mucin through regulating NF-${\kappa}B$ signaling pathway in airway epithelial cells.

Association of Hepatocyte Nuclear factor-4α Polymorphisms with Type 2 Diabetes in Koreans (한국인에서의 hepatocyte nuclear factor-4α의 유전자 다형성과 제2형 당뇨병과의 연관성)

  • Kim, Su-Won;Yoo, Min
    • Journal of Life Science
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    • v.19 no.3
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    • pp.362-365
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    • 2009
  • Type 2 diabetes is a typical polygenic disease complex, for which several common risk alleles have been identified. The hepatocyte nuclear factor-$4{\alpha}$ (HNF-$4{\alpha}$), a transcription factor involved in the regulation of serum lipid and glucose levels, has recently been associated with type 2 diabetes. Therefore, we investigated the genotype for the C>T polymorphism at position 12352 of the HNF-$4{\alpha}$ gene in Koreans and compared patient genotypes with those of the control group. 100 patients (63 males, 37 females) with a history of type 2 diabetes (T2DM) and 100 controls (36 males, 64 females) participated in this study. There was no association between 12352 C>T polymorphism in the HNF-$4{\alpha}$ gene and T2DM. The present study shows that HNF-$4{\alpha}$ 12352 C>T polymorphism may not be associated with the pathogenesis of T2DM. Further studies with larger populations may be needed for the development of diagnostic methods at a genetic level such as DNA chip.

Mechanisms Underlying Enterococcus faecalis-Induced Tumor Necrosis Factor-$\alpha$ Production in Macrophages

  • Choi, Eun-Kyoung;Kim, Dae-Eob;Oh, Won-Mann;Paek, Yun-Woong;Kang, In-Chol
    • International Journal of Oral Biology
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    • v.35 no.2
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    • pp.43-49
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    • 2010
  • Enterococcus faecalis, a gram-positive bacterium, has been implicated in endodontic infections, particularly in chronic apical periodontitis. Proinflammatory cytokines, including tumor necrosis factor-$\alpha$ (TNF-$\alpha$), are involved in the pathogenesis of these apical lesions. E. faecalis has been reported to stimulate macrophages to produce TNF-$\alpha$. The present study investigated the mechanisms involved in TNF-$\alpha$ production by a murine macrophage cell line, RAW 264.7 in response to exposure to E. faecalis. Both live and heat-killed E. faecalis induced high levels of gene expression and protein release of TNF-$\alpha$. Treatment of RAW 264.7 cells with cytochalasin D, an inhibitor of endocytosis, prevented the mRNA up-regulation of TNF-$\alpha$ by E. faecalis. In addition, antioxidant treatment reduced TNF-$\alpha$ production to baseline levels. Inhibition of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein (MAP) kinase also significantly attenuated E. faecalis-induced TNF-$\alpha$ expression by RAW 264.7 cells. Furthermore, activation of NF-${\kappa}B$ and AP-1 in RAW 264.7 cells was also stimulated by E. faecalis. These results suggest that the phagocytic uptake of bacteria is necessary for the induction of TNF-$\alpha$ in E. faecalis-stimulated macrophages, and that the underlying intracellular signaling pathways involve reactive oxygen species, ERK, p38 MAP kinase, NF-${\kappa}B$, and AP-1.