• Tuberculosis and Respiratory Diseases
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• v.49 no.3
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• pp.332-342
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• 2000

Background : The importance of pro-inflammatory cytokines, especially tumor necrosis factor $\alpha$ (INF-$\alpha$) and interleukin-1$\beta$ (IL-1$\beta$), have been extensively documented in the generation of inflammatory lung disease. Lung epithelial cells are also actively involved in initiating and maintaining inflammation by producing pro-inflammatory mediators. Understanding the mechanism of pro-inflammatory cytokine expression in lung epithelial cells is crucial to the development of new therapeutic modalities for inflammatory lung disease. Transcription of most pro-inflammatory cytokines is dependent on the activation of NF-${\kappa}B$. However, the relationship between pro-inflammatory cytokine expression and NF-${\kappa}B/I{\kappa}B$ pathway in lung epithelial cells is not clear. Methods : BEAS-2B, A549, Na-H157, NCI-H719 cells were stimulated with IL-$1{\beta}$ or TNF-$\alpha$ at various times, and then IL-8 and TNF-$\alpha$mRNA expressions were assayed by Northern blot analysis. IL-$1{\beta}$ or TNF-$\alpha$-induced NF-${\kappa}B$ activation was assessed by the nuclear translocation of p65 NF-${\kappa}B$ subunit. The degradation of $I{\kappa}B{\alpha}$ and $I{\kappa}B{\beta}$ by IL-$1{\beta}$ or TNF-$\alpha$stimulation was assayed by Western blot analysis. The phosphorylation of $I{\kappa}B{\alpha}$ was evaluated by Western blot analysis after pre-treating cells with proteasome inhibitor followed by IL-$1{\beta}$ or TNF-$\alpha$ stimulation. The basal level of IKK $\alpha$ expression was evaluated by Western blot analysis. Results: $I{\kappa}B{\alpha}$ and $I{\kappa}B{\alpha}$ was rapidly degraded after 5 minutes of incubation with IL-$1{\beta}$ or TNF-$\alpha$ in BEAS-2B, A549, and NCI-H157 cells. The activation of NF-${\kappa}B{\alpha}$ and the induction of IL-8 and TNF-$\alpha$ mRNA expression were observed by IL-$1{\beta}$ or TNF-$\alpha$ stimulation in these cells. In contrast, neither the changes in NF-${\kappa}B/I{\kappa}B$ pathway nor IL-8 and TNF-$\alpha$mRNA expression was induced by IL-$1{\beta}$ or TNF-$\alpha$ stimulation in NCI-H719 cells. IL-$1{\beta}$ and TNF-$\alpha$-induced $I{\kappa}B$ phosphorylation was observed in BEAS-2B, A549, and NCI-H157 cells, but not in NCI-H719 cells. The basal level of IKK$\alpha$ expression was not different between cell. Conclusion : NF-${\kappa}B/I{\kappa}B$ pathway plays an important role in the expression of pro-inflammatory cytokine in most lung epithelial cells. The absence of the effect on NF-${\kappa}B/I{\kappa}B$ pathway in NCI-H719 cells sæms to be due to the defect in the intracellular signal transduction pathway upstream to IKK.

• Korean Journal of Chemical Engineering
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• v.35 no.12
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• pp.2487-2495
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• 2018

Inspired by the specific amino acid sequence Asn-Pro-Ala (NPA) of water channel aquaporins (AQPs), we fabricated polyamide (PA) nanofiltration (NF) membranes by introducing reduced glutathione (GSH) in interfacial polymerization (IP) method. Fourier transform infrared spectroscopy (ATR-FTIR), X-ray photoelectron spectrometry (XPS), scanning electron microscope (SEM), atomic force microscopy (AFM), zeta potential and static water contact angle measurement were employed to characterize the chemical composition, morphology, electronegativity and hydrophilicity of the NF membranes. The water flux of GSH/PIP-TMC NF membrane reached $32.00L\;m^{-2}h^{-1}$ at 0.2 MPa, which was approximately twice than that of pristine PIP-TMC NF membrane when the ratio of GHS to piperazidine (PIP) was 40% during IP process. More water channels were built as GSH was embedded into PA layer. The fabricated NF membranes also took on potent rejection for dyes and $Na_2SO_4$. This study presents a simple and facile method to simulate water channels-based biological materials which may find potential application in water treatment.

• Proceedings of the Materials Research Society of Korea Conference
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• 1996.11a
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• pp.152-153
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• 1996

• Proceedings of the Materials Research Society of Korea Conference
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• 1997.10a
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• pp.55-55
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• 1997

• Parasites, Hosts and Diseases
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• v.52 no.5
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• pp.459-469
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• 2014

Entamoeba histolytica is a tissue-invasive protozoan parasite causing dysentery in humans. During infection of colonic tissues, amoebic trophozoites are able to kill host cells via apoptosis or necrosis, both of which trigger IL-8-mediated acute inflammatory responses. However, the signaling pathways involved in host cell death induced by E. histolytica have not yet been fully defined. In this study, we examined whether calpain plays a role in the cleavage of pro-survival transcription factors during cell death of colonic epithelial cells, induced by live E. histolytica trophozoites. Incubation with amoebic trophozoites induced activation of m-calpain in a time- and dose-dependent manner. Moreover, incubation with amoebae resulted in marked degradation of STAT proteins (STAT3 and STAT5) and NF-${\kappa}B$ (p65) in Caco-2 cells. However, $I{\kappa}B$, an inhibitor of NF-${\kappa}B$, was not cleaved in Caco-2 cells following adherence of E. histolytica. Entamoeba-induced cleavage of STAT proteins and NF-${\kappa}B$ was partially inhibited by pretreatment of cells with a cell-permeable calpain inhibitor, calpeptin. In contrast, E. histolytica did not induce cleavage of caspase-3 in Caco-2 cells. Furthermore, pretreatment of Caco-2 cells with a calpain inhibitor, calpeptin (but not the pan-caspase inhibitor, z-VAD-fmk) or m-calpain siRNA partially reduced Entamoeba-induced DNA fragmentation in Caco-2 cells. These results suggest that calpain plays an important role in E. histolytica-induced degradation of NF-${\kappa}B$ and STATs in colonic epithelial cells, which ultimately accelerates cell death.

• The Journal of Internal Korean Medicine
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• v.24 no.1
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• pp.113-122
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• 2003

Objective : The aim of this study was to evaluate the efficacy of Gagamchunggan-tang on anti-inflammation reaction with lipopolysaccharide (LPS)-induced HepG2 cell. Method : We examined the effects of the Gagamchunggan-tang, a traditional drug for liver inflammation, on the process of lipopolysaccharide(LPS)-induced nuclear factor-${\kappa}Bp65(NF-{\kappa}Bp65)$ activation in HepG2 cell. SDS-PAGE, Western blotting, Immunofluorescence staining were studied. Results : Immunoblot analysis showed that the level of nucleic $NF-{\kappa}Bp65$ was rapidly up-regulated and cytosolic inhibitory $I-{\kappa}B{\alpha}$ was down-regulated by LPS challenge. While Gagamchunggan-tang inhibited an increase of $NF-{\kappa}Bp65$ and degradation of $I-{\kappa}B{\alpha}$ in HepG2 cell. Besides LPS-induced expression of a group of genes, such as tumor necrosis factor-${\alpha}(TNF-{\alpha})$, inducible nitric oxide synthase(iNOS) and cyclooxygenase-2 (COX-2), are repressed by Gagamchunggan-tang. It may be concluded that Gagamchunggan-tang attenuates the progress of LPS-induced inflammation by reduction of $NF-{\kappa}Bp65$ activation. Conclusion : The Gagamchunggan-tang would be useful as a therapeutic agent for endotoxin-induced liver disease.

• Korean Journal of Pharmacognosy
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• v.39 no.2
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• pp.110-117
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• 2008

In this study, we investigated the anti-inflammatory effects of salidroside (SAL) isolated from the MeOH extract of Acer tegmentosum Maxim heartwood in RAW 264.7 macrophage cells. SAL pretreatment significantly inhibited nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$) productions in the lipopolysaccharide (LPS)-induced RAW 264.7 cells. Western blot and RT-PCR analyses revealed that SAL inhibited the LPS-induced expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the protein and mRNA levels in a concentration-dependent manner. In addition, SAL reduced the release and the mRNA expressions of tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) and interleukin-6 (IL-6). Furthermore, nuclear factorkappa B ($NF{-\kappa}B$) luciferase reporter assay was performed to know the involvement of SAL in the production of pro-inflammatory cytokines, we confirmed that LPS-induced transcription activity of $NF{-\kappa}B$ was inhibited by SAL. Taken together, our data indicate that anti-inflammatory property of salidroside might be the result from the inhibition of iNOS, COX-2, $TNF-{\alpha}$ and IL-6 expressions via the down-regulation of $NF{-\kappa}B$ activity.

• Molecules and Cells
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• v.43 no.2
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• pp.153-159
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• 2020

Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder. NF1 patients are predisposed to formation of several type solid tumors as well as to juvenile myelomonocytic leukemia. Loss of NF1 results in dysregulation of MAPK, PI3K and other signaling cascades, to promote cell proliferation and to inhibit cell apoptosis. The RUNX1 gene is associated with stem cell function in many tissues, and plays a key role in the fate of stem cells. Aberrant RUNX1 expression leads to context-dependent tumor development, in which RUNX1 may serve as a tumor suppressor or an oncogene in specific tissue contexts. The co-occurrence of mutation of NF1 and RUNX1 is detected rarely in several cancers and signaling downstream of RAS-MAPK can alter RUNX1 function. Whether aberrant RUNX1 expression contributes to NF1-related tumorigenesis is not fully understood. This review focuses on the role of RUNX1 in NF1-related tumors and blood disorders, and in sporadic cancers.

• KSII Transactions on Internet and Information Systems (TIIS)
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• v.16 no.10
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• pp.3333-3354
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• 2022

The 5G Core Network (5GC) is an essential part of the mobile communication network, but its security protection strategy based on the boundary construction is difficult to ensure the security inside the network. For example, the Network Function (NF) mutual authentication mechanism that relies on the transport layer security mechanism and OAuth2.0's Client Credentials cannot identify the hijacked NF. To address this problem, this paper proposes a trust model for 5GC based on NF interaction behavior to identify malicious NFs and improve the inherent security of 5GC. First, based on the interaction behavior and context awareness of NF, the trust between NFs is quantified through the frequency ratio of interaction behavior and the success rate of interaction behavior. Second, introduce trust transmit to make NF comprehensively refer to the trust evaluation results of other NFs. Last, classify the possible malicious behavior of NF and define the corresponding punishment mechanism. The experimental results show that the trust value of NFs converges to stable values, and the proposed trust model can effectively evaluate the trustworthiness of NFs and quickly and accurately identify different types of malicious NFs.

• Journal of Pharmacopuncture
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• v.6 no.2
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• pp.45-56
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• 2003

Objective : The purpose of this study was to investigate the effects of Bee Venom on the lipopolysaccharide(LPS), sodium nitroprusside(SNP), hydrogen peroxide$(H_2O_2)$-induced expression inducilble nitric oxide synthetase(iNOS), tumor necrosis factor-${\alpha}$(TNF-${\alpha}$) and nuclear factor kappa B(NF-kB) in RAW 264.7 cells, a murine macrophage cell line. Method : The expressions of expression iNOS and TNF-${\alpha}$ were determined by western blotting with corresponding antibodies. The expressions of expression NF-kB was assayed by EMSA method. Results : 1. The 0.5, 1 and $5{\mu}g/mg$ of bee venom on LPS-induced expression of iNOS, the $5{\mu}g/mg$ of bee venom on SNP-induced expression of iNOS and the $1{\mu}g/mg$ of bee venom on $H_2O_2$-induced expression of iNOS compared with control were inhibited significantly. 2. The 0.5, 1 and $5{\mu}g/mg$ of bee venom inhibited significantly LPS and $H_2O_2$-induced expression of TNF-${\alpha}$ compared with control, respectively. The $0.5{\mu}g/mg$ of bee venom increased significantly SNP-induced expression of TNF-${\alpha}$ compared with control. 3. The $5{\mu}g/mg$ of bee venom on LPS-induced expression of NF-kB, the $0.5{\mu}g/mg$ of bee venom on SNP-induced expression of NF-kB and the 0.5, $5{\mu}g/mg$ of bee venom on $H_2O_2$-induced expression of NF-kB were inhibited significantly compared with control, respectively.