• Journal of Marine Bioscience and Biotechnology
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• v.12 no.2
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• pp.99-107
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• 2020

Osteoarthritis (OA) is an inflammatory degenerative joint disease that is accompanied by irreversible joint cartilage destruction. Recently, the antioxidant effects of Carpomitra costata, which is a type of brown algae, have been reported, but their effects on OA have not been investigated. In this study, the anti-osteoarthritic effect of the ethanol extract of C. costata (EECC) on SW1353 human chondrocytes was studied. Results showed that EECC significantly attenuated the interleukin-1β (IL-1β)-induced release of pro-inflammatory mediators, including prostaglandin E2 and nitric oxide (NO), as well as expressions of cyclo-oxygenase-2 and inducible NO synthase. EECC also inhibited the IL-1β-induced expressions of matrix metalloproteinase-1, -3, and -13 in SW1353 chondrocytes, which reduced their extracellular secretion. In addition, the oxidative stress induced by IL-1β was confirmed to be blocked by EECC due to the inhibition of reactive oxygen species generation. Moreover, EECC suppressed IL-1β-mediated translocation of nuclear factor-kappa B (NF-κB) from cytosol into the nucleus and the degradation of IκB-α, which indicates that EECC exhibits anti-inflammatory effects by inhibiting the NF-κB signaling pathway. These results are the first to demonstrate the anti-inflammatory activities of C. costata extracts in chondrocytes, thus suggesting that this algae extract may be used in the treatment of OA.

• THE JOURNAL OF KOREAN ORIENTAL ONCOLOGY
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• v.5 no.1
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• pp.103-118
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• 1999

The activity of N-acetylglucosamitnyltransferase(GnT) III and V on a Melanoma B-16 was examined after incubation with interleukin 1 (IL-1). While augumenting cell proliferation, IL-1 resulted in a decrease of GnT-III activity and an increase of GnT-V activities. Consistant with this, Melanoma B-16 cultured with IL-1 showed increased affinlity to Daturam stramonium lectin, which recognizes asialo-tri- and asialeo-tetra-antenery N-linked oligosaccharides. These results indicate that IL-1 modulate glycosyltransferase activity and the oligosaccharide structure of target cells. On the other hand, to investigate whether or not TKM-SG affect GnT-V gene expression in lung metastatic carcinoma, we used RT-PCR methods. TKM-SG treated cell lines showed low levels of secretion of GnT-V mRNA transcription as elucidated by RT-PCR. Thus, with together lower GnT-V activity levels in the medium, TKM-SG was highly effective for lung cancer metastasis treatment and it was concluded that the medicine can be used as a potent anti-lung cancer metastasis medicine.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.4
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• pp.479-491
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• 1998

In order to know the pathogenesis of adult respiratory distress syndrome (ARDS) in association with the oxidative stress by neutrophils, the role of platelet activating factor (1-0-alkyl-2-acetyl-snglycero-3-phosphocholine, PAF) was investigated during acute lung injury induced by interleukin- $1{\alpha}$ (IL-1) in rats. An insufflation of IL-1 into the rat's trachea increased the acetyltransferase activity in the lung and the increase of PAF content was followed. As evidences of acute lung injury by neutrophilic respiratory burst, lung leak index, myeloperoxidase activity, numbers of neutrophils in the bronchoalveolar lavage fluid, neutrophilic adhesions to endothelial cells and NBT positive neutrophils were increased after IL-1 treatment. In addition, a direct instillation of PAF into the trachea caused acute lung leak and the experimental results showed a similar pattern in comparison with IL-1 induced acute lung injury. For the confirmation of oxidative stress during acute lung leak by IL-1 and PAF, a histochemical electron microscopy was performed. In IL-1 and PAF treated lungs of rats, the deposits of cerrous perhydroxide were found. To elucidate the role of PAF, an intravenous injection of PAF receptor antagonist, WEB 2086 was given immediately after IL-1 or PAF treatment. WEB 2086 decreased the production of hydrogen peroxide and the acute lung leak. In ultrastructural study, WEB 2086 mitigated the pathological changes induced by IL-1 or PAF. The nuclear factor kappa B (NFkB) was activated by PAF and this activation was inhibited by WEB 2086 almost completely. Based on these experimental results, it is suggested that the PAF produced in response to IL-1 through the remodeling pathway has the major role for acute lung injury by neutrophilic respiratory burst. In an additional experiment, we can also come to conclude that the activation of the NFkB by PAF is thought to be the fundamental mechanism to initiate the oxidative stress by neutrophils causing release of proinflammatory cytokines and activation of phospholipase $A_2$.

• Proceedings of the KSAR Conference
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• 2003.06a
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• pp.52-52
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• 2003

Granulocyte-macrophage colony stimulating factor (GM-CSF) is synthesized in the female reproductive tract and has been shown to play an important role in human and murine embryo development and implantation. However, the mechanism of GM-CSF on the embryo development is unknown. Recent studies suggested that GM-CSF may be increase the expression of implantation relented genes, such as interleukin-1 (IL-1) system. Our aim of this study was to compare the interleukin-1$\alpha$ (IL-1$\alpha$), interleukin-1$\beta$ (IL-1$\beta$) and interleukin-1 receptor antagonist (IL-lra) mRNA between the GM-CSF supplemented group and control group in mouse embryos. Mouse 2-cell embryos were cultured in P-1 medium supplemented with or without mouse GM-CSF (10 ng/ml). The number of total and apoptotic cell in blastocyst were assessed by TUNEL. And then, the expression of IL-1$\alpha$, IL-1$\beta$ and IL-1ra mRNA in blastocyst were examined by RT-PCR.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.5
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• pp.2395-2399
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• 2016

Background: Hepatitis B virus (HBV) is a major risk factor for hepatocellular carcinoma (HCC). Cytokines play an important role in the regulation of immune responses and defense against viral infections. Human interleukin 6 (IL6) is a multifunctional cytokine that participates in these processes. Objective: The aim of this study was to assess the IL6-174 gene polymorphism in patients with chronic hepatitis B virus (HBV) infection as compared with healthy controls in an Iranian population. Materials and Methods: Totals of 297 HBV patients and 368 control individuals were evaluated. Genomic DNA was extracted from peripheral blood and the SSP-PCR (sequence specific primer-polymerase chain reaction) method was applied for genotyping. Results: The frequencies of genotypes C/C, G/G and C/G in HBV cases were 4.7%, 34.3%, 60.9% and in controls were 12.8%, 39.7% and 47.6%, respectively. The frequencies of G and C allele in patients and controls were 78.1%, 21.9% and 67.4%, 32.6 % respectively. There was a significant difference in the frequencies of G/G genotype (CI=1.8-7.1, OR=3.47, P=0.00001) and G allele (CI=1.34-2.23, OR=1.72, P=0.0001) between HBV patients and the control group. Conclusions: These findings suggest that the IL6-174 C/G genotype and the G allele are strongly associated with susceptibility to HBV infection. Demographic information showed that most of the subjects were male (74.4%). According to high frequency of G/G genotype in male participants (63.1%) men probably are more susceptible to hepatitis than women.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.23 no.1
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• pp.44-58
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• 2010

Silibinin is the major active molecule of silymarin, the mixture of flavonolignans extracted from Cirsium japonicum (CJ). It has been used for treatment of hepatitis and inflammation related diseases. The aim of this study was to prove whether Silibinin has effectiveness for allergic inflammation. Silibinin processes the inflammatory reaction in phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187 (PMA plus A23187) stimulated human mast cell line (HMC-1). Its effect was examined by ELISA, RT-PCR, Western blot, and Luciferase assay. The results were Silibinin inhibited the expression of histamine, TNF-$\alpha$ (tumor necrosis factor-$\alpha$), IL-6 (interleukin-6), and IL-8 (interleukin-8). Silibinin suppressed NF-${\kappa}B$ (nuclear factor kappa B) activation in stimulated HMC-1 (human mast cell-1). This effect was mediated through inhibition of phosphorylation and degradation of $IkB{\alpha}$, an inhibitor of NF-kB. Silibinin significantly inhibited induction of NF-kB promoter mediated Luciferase assay. These results suggest that Silibinin has a potential molecule for therapy of mast cell-derived allergic inflammatory diseases.

• Molecules and Cells
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• v.43 no.5
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• pp.479-490
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• 2020

Interleukin-9 (IL-9) is well known for its role in allergic inflammation. For cancer, both pro- and anti-tumor effects of IL-9 were controversially reported, but the impact of IL-9 on tumor metastasis has not yet been clarified. In this study, IL-9 was expressed as a secretory form (sIL-9) and a membrane-bound form (mbIL-9) on B16F10 melanoma cells. The mbIL-9 was engineered as a chimeric protein with the transmembrane and cytoplasmic region of TNF-α. The effect of either mbIL-9 or sIL-9 expressing cells were analyzed on the metastasis capability of the cancer cells. After three weeks of tumor implantation into C57BL/6 mice through the tail vein, the number of tumor modules in lungs injected with IL-9 expressing B16F10 was 5-fold less than that of control groups. The percentages of CD4⁺ T cells, CD8⁺ T cells, NK cells, and M1 macrophages considerably increased in the lungs of the mice injected with IL-9 expressing cells. Among them, the M1 macrophage subset was the most significantly enhanced. Furthermore, peritoneal macrophages, which were stimulated with either sIL-9 or mbIL-9 expressing transfectant, exerted higher anti-tumor cytotoxicity compared with that of the mock control. The IL-9-stimulated peritoneal macrophages were highly polarized to M1 phenotype. Stimulation of RAW264.7 macrophages with sIL-9 or mbIL-9 expressing cells also significantly increased the cytotoxicity of those macrophages against wild-type B16F10 cells. These results clearly demonstrate that IL-9 can induce an anti-metastasis effect by enhancing the polarization and proliferation of M1 macrophages.

• Advances in Traditional Medicine
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• v.5 no.4
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• pp.251-261
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• 2005

Rheumatoid arthritis (RA) is an autoimmune/inflammatory disorder with a complex genetic component. RA is characterized by chronic inflammation of the synovial membrane in the joint, which leads to the progressive destruction of articular cartilage, ligament and bone. Several cytokines such as tumor necrosis $factor-{\alpha}\;TNF-{\alpha}\;and\;interleukin-1{\beta}\;(IL-1{\beta})$ and interleukin-6 (IL-6) have been implicated in the pathological mechanisms of synovial tissue proliferation, joint destruction and programmed cell death in rheumatoid joint. Genome wide screening of subjects suffering from autoimmune diseases especially arthritis revealed linkage to inflammatory molecules like $TNF-{\alpha},\;IL-1{\beta}$ and IL-6, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor-kappaB $(NF-{\kappa}B)$ and human leucocyte antigen/major histocompatibility complex (HLA/MHC) locus. The status of the pharmacological mechanism of herbal drugs in the light of genome wide screening results has been discussed to reinforce the therapeutic potential and the pharmacological basis of the herbal drugs.

• Natural Product Sciences
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• v.21 no.4
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• pp.240-247
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• 2015

Viridicatol (1) has previously been isolated from the extract of the marine-derived fungus Penicillium sp. SF-5295. In the course of further biological evaluation of this quinolone alkaloid, anti-inflammatory effect of 1 in RAW264.7 and BV2 cells stimulated with lipopolysaccharide (LPS) was observed. In this study, our data indicated that 1 suppressed the expression of well-known pro-inflammatory mediators such as inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, and consequently inhibited the production of iNOS-derived nitric oxide (NO) and COX-2-derived prostaglandin E2 ($PGE_2$) in LPS stimulated RAW264.7 and BV2 cells. Compound 1 also reduced mRNA expression of pro-inflammatory cytokines such as $interleukin-1{\beta}$ ($IL-1{\beta}$), interleukin-6 (IL-6), and tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$). In the further evaluation of the mechanisms of these anti-inflammatory effects, 1 was shown to inhibit nuclear factor-kappa B ($NF-{\kappa}B$) pathway in LPS-stimulated RAW264.7 and BV2 cells. Compound 1 blocked the phosphorylation and degradation of inhibitor kappa B $(I{\kappa}B)-{\alpha}$ in the cytoplasm, and suppressed the translocation of $NF-{\kappa}B$ p65 and p50 heterodimer in nucleus. In addition, viridicatol (1) attenuated the DNA-binding activity of $NF-{\kappa}B$ in LPS-stimulated RAW264.7 and BV2 cells.

• Journal of Life Science
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• v.19 no.4
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• pp.514-519
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• 2009

Monocyte chemoattractant protein 1 (MCP1) plays a key role in monocyte /macrophage infiltration to the sub-endothelial space of the blood vessel wall, which is a critical initial step in atherosclerosis. In this study, we examined $interleukin-1{\bate}$ ($IL-1{\beta}$) induced MCP1 expressions via activation of transcription factor $NF-{\kappa}B$ in primary human aorta smooth muscle cells. We determined the effect of several anti-inflammatory agents on $IL-1{\beta}-induced$ MCP1 expression. The pretreatment of luteolin significantly suppressed $IL-1{\beta}-induced$ MCP1 expressions through blocking activation and translocation of $NF-{\kappa}B$ to the nucleus.