• Title/Summary/Keyword: interleukin-1 beta

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The effect of Oligonol intake on cortisol and related cytokines in healthy young men

  • Lee, Jeong-Beom;Shin, Young-Oh;Min, Young-Ki;Yang, Hun-Mo
    • Nutrition Research and Practice
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    • v.4 no.3
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    • pp.203-207
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    • 2010
  • This study investigated the effects of Oligonol intake on cortisol, interleukin (IL)-$1{\beta}$, and IL-6 concentrations in the serum at rest and after physical exercise loading. Nineteen healthy sedentary male volunteers participated in this study. The physical characteristics of the subjects were: a mean height of $174.2{\pm}2.7$ cm, a mean weight of $74.8{\pm}3.6$ kg and a mean age of $22.8{\pm}1.3$ years. Each subject received 0.5 L water with Oligonol (100 mg/day) (n = 10) or a placebo (n = 9) daily for four weeks. The body composition, the white blood cell (WBC) and differential counts as well as the serum cortisol, IL-$1{\beta}$, and IL-6 concentrations were measured before and after Oligonol intake. The cortisol concentration and serum levels of IL-$1{\beta}$ and IL-6 after Oligonol intake were significantly decreased compared to before treatment (P < 0.01, respectively). In addition, the rate of increase of these factors after exercise was decreased compared to the placebo group. There was no change in the WBC and differential cell counts. These results suggest that oral Oligonol intake for four weeks had a significant effect on inhibition of inflammatory markers in healthy young men.

Regulation of Interleukin-1${\beta}$-induced Dedifferentiation and Apoptosis via p38 Mitogen-activated Protein Kinase Pathway in Articular Chondnocytes (연골세포의 탈분화 및 세포고사 억제를 위한 기전연구)

  • Huh Jeong-Eun;Cho Eun-Mi;Yang Ha-Ru;Kim Dae-Sung;Baek Yong-Hyeon;Lee Jae-Dong;Choi Do-Young;Park Dong-Suk
    • The Journal of Korean Medicine
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    • v.27 no.1 s.65
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    • pp.220-228
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    • 2006
  • Objectives : Interleukin-1 (IL-1)${\beta}$ in articular chondrocytes regulates differentiation, apoptosis, and inflammatory responses. It is still controversial, So, we investigated IL- $1{\beta}$ induces chondrocytes dedifferentiation and death. Also, we studied the role of the mitogen-activated protein kinase (MAPK) subtypes on IL-$1{\beta}$-induced dedifferentiation and apoptosis. Methods : To evaluation of dedifferentiation by chemokines of chondrocytes, we assessed such as proteoglycan, collagen, MMP-3 and MMP-13 by RT-PCR analysis. Also, to assess of apoptosis effect by chemokines, we measured annexin V/propidium iodode (PI) and sub G1 cells in chondrocytes by flowcytometric analysis Results : IL-$1{\beta}$ treatment did not affect activation of ERK-1/2, but stimulation of p38 kinase. Inhibition of phospho ERK-1/2 with PD98059 enhanced IL-1b-induced dedifferentiation, and apoptosis up to 13.5%, whereas inhibition of phospho p38 kinase with SB203580 inhibited dedifferentiation, and apoptosis. Conclusions : Our results indicate that SB203580, p38 kinase inhibitor, inhibits IL-$1{\beta}$-induced dedifferentiation, and apoptosis by the inhibition of type II collagen expression and proteoglycan synthesis of rabbit articular chondrocytes.

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The Effect of Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) on The Expression of IL-1 System mRNA in Mouse Embryos

  • Kim, D. H.;S. S. Ko;Lee, H. C.;Lee, H. H.;Kim, S. S.;Lee, H. J.;B. C. Yang;Park, S. B.;W. K. Chang
    • 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.

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Serum interleukin-1beta and tumor necrosis factor-alpha in febrile seizures: is there a link?

  • Mahyar, Abolfazl;Ayazi, Parviz;Orangpour, Reza;Daneshi-Kohan, Mohammad Mahdi;Sarokhani, Mohammad Reza;Javadi, Amir;Habibi, Morteza;Talebi-Bakhshayesh, Mousa
    • Clinical and Experimental Pediatrics
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    • v.57 no.10
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    • pp.440-444
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    • 2014
  • Purpose: Febrile seizures are induced by fever and are the most common type of seizures in children. Although numerous studies have been performed on febrile seizures, their pathophysiology remains unclear. Recent studies have shown that cytokines may play a role in the pathogenesis of febrile seizures. The present study was conducted to identify potential links between serum interleukin-1beta (IL-$1{\beta}$), tumor necrosis factor-alpha (TNF-${\alpha}$), and febrile seizures. Methods: Ninety-two patients with simple or complex febrile seizures (46 patients per seizure type), and 46 controls with comparable age, sex, and severity of temperature were enrolled. Results: The median concentrations of serum IL-$1{\beta}$ in the simple, complex febrile seizure, and control groups were 0.05, 0.1, and 0.67 pg/mL, respectively (P=0.001). Moreover, the median concentrations of TNF-${\alpha}$ in the simple, complex febrile seizure, and control groups were 2.5, 1, and 61.5 pg/mL, respectively (P=0.001). Furthermore, there were significant differences between the case groups in serum IL-$1{\beta}$ and TNF-${\alpha}$ levels (P<0.05). Conclusion: Unlike previous studies, our study does not support the hypothesis that increased IL-$1{\beta}$ and TNF-${\alpha}$ production is involved in the pathogenesis of febrile seizures.

CD Gene Microarray Profiles of Bambusae Caulis in Liquamen in Human Mast Cell

  • Jeon Hoon;Kang Nan Joo;Kim Gyo Seok
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.17 no.1
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    • pp.241-246
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    • 2003
  • Bambusae Caulis in Liquamen(BCL) has been used to relieve the cough and asthma, and remove the phlegm in traditional Oriental medicine. In recent years, it was studied for its antiinflammatory, antiallergenic, immune-modulating, and anticarcinogenic capabilities. This experiment was performed to evaluate the microarray profiles of CD genes in human mast cells before and after BCL treatment. The results are as follows: The expression of 51 of the genes studied was up-regulated in the Bel-treated group; they include the genes coding L apoferritin, beta-2-microglobulin, ferritin light polypeptide, CD63, monocyte chemotactic and activating fact, heme oxygenase 1, CD140a, integrin alpha M, colony stimulating factor 2 receptor, eukaryotic translation elongation factor, CD37, interleukin 18, NADH dehydrogenase 1 beta, CD48, 5-lipoxygenase activating protein, interleukin 4, ribosomal protein L5, GABA(A) receptor-associated protein, beta-tubulin, integrin beta 1, CD162, CD32, lymphotoxin beta, alpha-tublin, integrin alpha L, CD2, CD151, CD331, 90 kDa heat shock protein, CD59, CD3Z, microsomal glutathione S-transferase 2, CD33, CD162R, cyclophilinA, CD84, interleukin 9 receptor, interleukin 11, CD117, CD39-Like 2, and so forth. The expression of 7 of the genes studied was down-regulated in the BCL-treated group; they include the genes coding con, CD238, SCF, CD160, CD231, CD24, and CD130. Consequently, the treatment of BCL on the human mast cells increased the expression of 51 genes and decreased the expression of 7 genes. These data would provide a fundamental basis to the traditional applications of Bambusae Caulis in Liquamen.

Polymorphisms of interleukin-1β promoter in simple febrile seizures (단순 열성 경련에서 interleukin-1β promoter 유전자의 다형성)

  • Yoon, Jang Won;Choen, Eun Jung;Lee, Young Hyuk
    • Clinical and Experimental Pediatrics
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    • v.51 no.9
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    • pp.1007-1011
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    • 2008
  • Purpose : Febrile seizure (FS) is the most common type of seizure. The role of genetic factors in FSs has long been recognized. A positive family history can be elicited in 25-40% of patients with FSs; nonetheless, the genes responsible for FSs in the majority of the population remain unknown. Interleukin-$1{\beta}$ ($IL-1{\beta}$) is a pro-inflammatory cytokine that acts as an endogenous pyrogen. Thus, $IL-1{\beta}$ could be involved in the pathophysiology of FSs. Methods : To determine whether or not single nucleotide polymorphisms of the $IL-1{\beta}$ gene are associated with susceptibility to simple FSs, $IL-1{\beta}$ promoter -31 and -511 genotyping was performed by means of polymerase chain reaction-restriction fragment (PCR-RF) length polymorphism in 40 FS patients (20 sporadic and 20 familial FS patients) and 33 controls. Results : There were no significant differences in the frequencies of -31 C/T and -511 C/T in the $IL-1{\beta}$ promoter gene, between simple FS patients and controls. Conclusion : The frequency of CT/CT increased relatively in familial FS patients. A study examining a larger number of FS patients is needed.

Mycobacterium tuberculosis-induced Expression of Interleukin-1 Beta is Mediated Via Protein Kinase C Signaling Pathway

  • Cho, Jang-Eun;Lee, Kyung-Hong;Son, Sin-Jee;Park, Sang-Jung;Lee, Hye-Young;Kim, Yoon-Suk
    • Biomedical Science Letters
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    • v.16 no.2
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    • pp.119-122
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    • 2010
  • Interleukin-1${\beta}$ $(IL-1{\beta})$ is one of the key proinflammatory cytokines and it plays an important role for the antimycobacterial host defense mechanisms. In this study, we examined Mycobacterium tuberculosis (MTB)-stimulated induction of IL-1${\beta}$ and evaluated the associated signal transduction pathways. In PMA-differentiated THP-1 cells, MTB infection increased mRNA expression of IL-$1{\beta}$ in a dose-dependent manner. The expression of IL-1${\beta}$ mRNA began to be induced at 1.5 h after infection, and induced expression of IL-1${\beta}$ was retained for 48 h after MTB infection. The increase in expression of IL-1${\beta}$ caused by MTB was reduced in cells treated with Ro-31-8425 (an inhibitor of PK$C{\alpha}$, ${\beta}I$, ${\beta}II$, ${\gamma}$, ${\varepsilon}$) or PD98059 (an inhibitor of MEK1), meanwhile, pre-treatment with $G\ddot{o}6976$ (an inhibitor of $Ca^{2+}$ dependent PK$C{\alpha}$ and PK$C{\beta}I$) or Rottlerin (an inhibitor of PK$C{\delta}$) has no effect on MTB-induced expression of $IL-1{\beta}$ mRNA. These results show that the expression of $IL-1{\beta}$ mRNA caused by MTB may be mediated via MEK1 and PKC isoforms including PK$C{\beta}II$, $PKC{\gamma}$, or $PKC{\varepsilon}$. Further studies are required to determine whether other PKC isoforms $(PKC {\eta},\;{\theta},\;{\varepsilon},\;and\;{\lambda}/{\iota})$, except $PKC{\delta}$, $PKC{\alpha}$, and $PKC{\beta}I$, are also involved in $IL-1{\beta}$ mRNA expression after mycobacterial infection.

The Effect of Jeongshin-tang on Interleukin-1 $\beta$ and $\beta$-Amyloid-Induced Cytokine Production in Human Brain Astrocytes

  • Kim Bo Kyung;Shin Soon Shik;Kang Seon Tae
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.18 no.1
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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.

I)Interleukin-1 수용체 길항제에 의한 만성골수성백혈병 집락형성 및 K562 증식억제 II)각종 암세포주에 대한 P항암제의 항암효과

  • 김삼용
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 1994.04a
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    • pp.207-207
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    • 1994
  • I) 지금까지 만성골수성백혈병의 치료법으로서 골수이식이나 인터페론의 투여등이 시행되어왔으며 백혈병세포에서 Interleukin-1$\beta$(이하 IL-1$\beta$)이 자율적으로 생성됨이 보고 되어 이러한 질병의 진행에 IL-1$\beta$의 활성증가가 관련될것이라는 견해가 대두되어 왔다. 최근 단핵구성백혈병 환자의 소변에서 분리된 IL-1수용체 길항제(1L-1 receptor antagonist: IL-lRA)가 clonig되었고 인터페론치료에 저항하는 환자들의 치료에 IL-1RA 가 이용될수 있을것이라는 견해가 있다. 따라서 본 연구는 유전공학연구소가 분리 정제한 IL-1RA가 만성골수백혈병 환자로부터 유래한 K562세포주의 증식에 미치는 영향을 평가하고 알파인터페론과의 병용투여시의 상호작용에 관해 검토하였다.

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