• BMB Reports
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• 제45권7호
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• pp.414-418
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• 2012

Triglycerides (TG) are implicated in the development of atherosclerosis through formation of foam cells and induction of macrophage cell death. In this study, we report that addition of exogenous TG induced cell death in phorbol 12-myristate 13-acetate-differentiated THP-1 human macrophages. TG treatment induced a dramatic decrease in interleukin-$1{\beta}$ (IL-$1{\beta}$) mRNA expression in a dose- and time-dependent manner. The expression of granulocyte macrophage colony-stimulating factor and platelet endothelial cell adhesion molecule remained unchanged. To identify signaling pathways involved in TG-induced downregulation of IL-$1{\beta}$, we added p38 MAPK, protein kinase C (PKC) or c-Raf1 specific inhibitors. We found that inhibition of p38 MAPK alleviated the TG-induced downregulation of IL-$1{\beta}$, whereas inhibition of PKC and c-Raf1 had no effect. This is the first report showing decreased IL-$1{\beta}$ expression during TG-induced cell death in a human macrophage line. Our results suggest that downregulation of IL-$1{\beta}$ expression by TG-treated macrophages may play a role during atherogenesis.

• 대한치과보존학회:학술대회논문집
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• 대한치과보존학회 2003년도 제120회 추계학술대회 제 5차 한ㆍ일 치과보존학회 공동학술대회
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• pp.621-621
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• 2003

I. Objectives In order to examine the immunoresponse of host cells to Enterococcus faecalis, this in vitro study monitored the production of Interleukin-2(IL-2), Interleukin-4(IL-4) and Transforming growth $factor-{\beta}1(TGF-{\beta}1)$ in human lymphocytes. II. Materials and methods Enterococcus faecalis(ATCC29212) strains were used in this study. Strains were grown in 1-liter cultures in 85% N2-10% H2-5% $CO_2$chamber for 3 days at $37^{\circ}C$. The medium used was 3.7% brain heart infusion broth. Bacterial cells harvested from 1-liter cultures were washed, suspended in 20ml of phosphate-buffered saline(PBS). Suspensions of bacterial cells were disrupted by sonication on ice for 5 min. Protein concentration was determined by the Bicinchoninic acid(BCA) protein assay.(omitted)

• 대한수의학회지
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• 제50권2호
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• pp.79-84
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• 2010

The molecule possessing ankyrin-repeats induced by lipopolysaccharide (MAIL) protein is a novel member of the $Ikappa{\beta}$ family. In the present study, we examined the effect of norepinephrine (NE) on MAIL mRNA expression in primary cultured mouse hepatocytes and non-parenchymal liver cells. MAIL mRNA expression in hepatocytes and non-parenchymal liver cells was not directly influenced by NE. However, MAIL mRNA expression in hepatocytes was significantly induced by incubation with a culture medium of non-parenchymal liver cells, treated with NE. Pretreatment with an interleukin (IL)-1 receptor antagonist significantly attenuated the stimulatory effect of the medium. Moreover, exogenous $IL-1{\beta}$ induced MAIL mRNA expression in hepatocytes, while IL-6 and tumor necrosis factor $\alpha$ did not. The concentration of $IL-1{\beta}$ in the medium of non-parenchymal liver cells was significantly increased after NE-treatment. These results suggest that NE can induce MAIL mRNA expression in hepatocytes through $IL-1{\beta}$, released from non-parenchymal liver cells.

• 대한한방내과학회지
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• 제25권3호
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• pp.398-407
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• 2004

목적 :천축황(天竺黃)이 골대사에 미치는 영향을 검토하고자 생쥐의 골세포를 이용하여 골흡수 억제 효과를 관찰하였다. 방법 :$Interleukin-1{\beta}\;(IL-1{\beta})$는 시험관내에서 osteoblast를 조절하는 것으로 알려져 있는데, 천축황(天竺黃)이 $IL-1{\beta}$ 유발된 $PGE_2$, 생성에 관한 영향을 관찰하였다. 결과 :천축황(天竺黃)는 osteoblast체 독성을 나타내지 않았으며, $PGE_2$ 생성을 억제하였다. 특히, 천축황(天竺黃)을 1시간동안 전처리한 경우 $PGE_2$의 합성을 억제하여 골세포 보호효과가 인정되었으며, 또한 골 흡수인자인 $IL-1{\beta}$에 의해 유발된 alkaline phosphatase의 활성도 억제하였는데, 천축황(天竺黃) 전처리후 16시간째에 훨씬 높은 억제효과를 나타내었다. 유사하게 천축황(天竺黃)을 1시간 동안 전처리한 경우 osteocalcin의 생성이 증가되었다. 또한, calcitonin이 나타내는 osteoclast및 osteoblast 함유세포에서 골 흡수를 억제하였다. 결론 :천축황(天竺黃)은 osteoclast가 매개된 골흡수를 억제하는 효과가 인정되었다.

• 대한한방부인과학회지
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• 제22권3호
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• pp.83-98
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• 2009

Purpose: This study was performed to evaluate the anti-inflammatory effect of Eungapbang extract (EGB). Methods: To evaluate the anti-inflammatory effects of EGB, we nourished RAW 264.7 cell lines in the laboratory dish. Next, inflammatory cytokine concentrations were analyzed. Then, sera were prepared from blood after lipopolysaccharide (LPS) injection in chemically induced mouse models of intestinal inflammation, and Interleukin-1${\beta}$ (IL-1${\beta}$), interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF-${\alpha}$) were measured using ELISA kits. Results: 1. EGB significantly suppressed the expression levels of IL-1${\beta}$ and NOS-II genes at 100, 50 and 10 ${\mu}g/m{\ell}$ concentrations, and IL-6, TNF-${\alpha}$ and COX-2 mRNAs at 100 and 50 ${\mu}g/m{\ell}$ concentrations. 2. EGB significantly reduced the production level of IL-1${\beta}$ and TNF-${\alpha}$ at 100${\mu}g/m{\ell}$ concentrations, and IL-6 at 100 and 50 ${\mu}g/m{\ell}$ concentrations. 3. EGB significantly decreased the production level of IL-1${\beta}$ and IL-6 in sera of acute inflammation induced mice. 4. EGB could suppress the expression level of IL-1${\beta}$ and IL-6 mRNA in spleen tissues in acute inflammation induced mice. Conclusion: On the basis of the above results, it is confirmed that the anti-inflammatory effects of EGB were recognized. Therefore, EGB is recommended as promising therapy for treatment of such ailments as pelvic inflammatory disease.

• International Journal of Oral Biology
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• 제34권1호
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• pp.1-6
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• 2009

The purpose of the present study was to examine the role of peripheral nitric oxide (NO) pathways in the onset of interleukin (IL)-1$\beta$-induced mechanical allodynia in the orofacial area. Experiments were carried out on male Sprague-Dawley rats weighing 230-280 gm and surgical procedures were performed under pentobarbital sodium (40 mg/kg, i.p.). Under anesthesia, a polyethylene tube (PE10) was implanted into the subcutaneous area of one vibrissa pad, which enabled the injection of IL-1$\beta$ or other chemicals. We subcutaneously injected 50 ${\mu}L$ of IL-1$\beta$ into a vibrissa pad through the implanted polyethylene tube with a 100 ${\mu}L$ Hamilton syringe. After the administration of 0.01, 0.1, 1, or 10 pg of IL-1$\beta$, withdrawal behavioral responses were examined. The subcutaneous injection of saline had no effects on the air-puff thresholds. Following the subcutaneous injection of 0.01, 0.1, 1, or 10 pg of IL-1$\beta$, the threshold of air puffs decreased significantly to 12 $\pm$ 3, 7 $\pm$ 2, 5 $\pm$ 1, or 5 $\pm$ 1 psi, respectively, in a dose dependent manner. Pretreatment with L-NAME, a nitric oxide synthase (NOS) inhibitor, blocked IL-1$\beta$-induced mechanical allodynia. However, neither D-NAME, an inactive isomer of L-NAME, nor vehicle affected the IL-1$\beta$-induced mechanical allodynia. Subcutaneous injection of IL-1$\beta$ increased the number of c-fos-like immunoreactive neurons, whereas pretreatment with L-NAME decreased this number, in the trigeminal caudal nucleus. These results suggest that pro-inflammatory cytokines and NO are important contributors to the pathogenesis of persistent and exaggerated IL-1$\beta$-induced pain states. Based on these observations, peripheral application of NOS inhibitors may be of therapeutic value in treating pain disorders in the clinic.

• International Journal of Oral Biology
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• 제41권4호
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• pp.237-242
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• 2016

Interleukin-1b ($IL-1{\beta}$), a proinflammatory cytokine, regulates the innate immune responses against bacterial infection. Mature $IL-1{\beta}$ is produced from $pro-IL-1{\beta}$ by activated caspase-1, which in turn is activated by the inflammasome complex formation. In this study, we compared the inflammasome mRNA expression induced by S. sanguinis, S. oralis, F. nucleatum and P. intermedia. Among the tested bacteria, S. sanguinis induced the highest $IL-1{\beta}$ secretion. S. oralis, F. nucleatum and P. intermedia induced very weak $IL-1{\beta}$ secretion. S. sanguinis mostly induced the NLRP3 mRNA expressions. Although F. nucleatum did not induce high $IL-1{\beta}$ secretion, it induced high expression levels of AIM2, NLRP2, and NLRP3. No specific inflammasomes were induced by S. oralis and P.intermedia. Studying the inflammasome complex activation induced by oral bacteria may thus enhance our understanding of the pathogenesis of oral diseases.

• Archives of Pharmacal Research
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• 제28권5호
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• pp.582-586
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• 2005

The present study was designed to characterize the possible roles of spinally located cholera toxin (CTX)- and pertussis toxin (PTX)-sensitive G-proteins in pro- inflammatory cy tokine induced pain behaviors. Intrathecal injection of tumor necrosis factor-a (TNF-${\alpha}$; 100 pg), interleukin-1${\beta}$ (IL-1${\beta}$ 100 pg) and interferon-${\gamma}$ (INF-${\gamma}$; 100 pg) showed pain behavior. Intrathecal pretreatment with CTX (0.05, 0.1 and 0.5 mg) attenuated pain behavior induced by TNF-${\alpha}$ and INF-${\gamma}$ administered intrathecally. But intrathecal pretreatment with CTX (0.05, 0.1 and 0.5${\mu}g$) did not attenuate pain behavior induced by IL-1${\beta}$. On the other hand, intrathecal pretreatment with PTX further increased the pain behavior induced by TNF-${\alpha}$ and IL-1${\beta}$ administered intrathecally, especially at the dose of 0.5 ${\mu}g$. But intrathecal pretreatment with PTX did not affect pain behavior induced by INF-${\gamma}$. Our results suggest that, at the spinal cord level, CTX- and PTX-sensitive G-proteins appear to play important roles in modulating pain behavior induced by pro-inflammatory cytokines administered spinally. Furthermore, TNF-${\alpha}$, IL-1${\beta}$ arid INF-${\gamma}$ administered spinally appear to produce pain behavior by different mechanisms.

• 동의생리병리학회지
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• 제18권1호
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• pp.254-259
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• 2004

Jeongshin-tang (JST) is a Korean herbal prescription, which has been successfully applied for the various neuronal diseases. However, it's effect remains unknown in experimental models. To investigate the biological effect of JST in Alzheimer's disease (AD) in vitro model, we analized the production of interleukin (IL)-6 and IL-8, and expression of cyclooxygenase (COX)-2 in IL-1β plus β-amyloid [25-35] fragment (A)-stimulated human astrocytoma cell line U373MG. JST alone had no effect on the cell viability. The production of IL-6 and IL-8 was significantly inhibited by pretreatment with JST (1mg/㎖) on IL-1β plus A-stimulated U373MG cells. Maximal inhibition rate of IL-6 and IL-8 production by JST was about 41.22% (P<0.01) and 34.45% (P<0.05), respectively. The expression level of COX-2 protein was up-regulated by IL-1β plus A but the increased level of COX-2 was inhibited by pretreatment with JST (1 mg/㎖). These data indicate that JST has a regulatory effect on cytokine production and COX-2 expression, which might explain it's beneficial effect in the treatment of AD.

• Advances in Traditional Medicine
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• 제5권4호
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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.