• Title/Summary/Keyword: IL-1 beta

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Activation of $PPAR{\alpha}$ Attenuates $IFNP{\gamma}$ and IL-$1{\beta}$-induced Cell Proliferation in Astrocytes: Involvement of IL-6 Independent Pathway

  • Lee, Jin-Koo;Seo, Eun-Min;Lee, Sang-Soo;Park, Soo-Hyun;Sim, Yun-Beom;Jung, Jun-Suh;Kim, Seon-Mi;Suh, Hong-Won
    • The Korean Journal of Physiology and Pharmacology
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    • v.14 no.3
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    • pp.185-189
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    • 2010
  • The present study demonstrates the effect of fibrates, agonists of $PPAR{\alpha}$ on cytokines-induced proliferation in primary cultured astrocytes. Alone or combination treatment with cytokines, such as IL-$1{\beta}$ (10 ng/ml), $IFNP{\gamma}$ (10 ng/ml), and TNF-$\alpha$ (10 ng/ml) cause a significant increase of cell proliferation in a time-dependent manner. Treatment of astrocytes with bezafibrate and fenofibrate (0, 5, and $10\;{\mu}M$) reduced the $IFNP{\gamma}$ and IL-$1{\beta}$-induced cell proliferation in a dose-dependent manner. To address the involvement of IL-6 on the $IFNP{\gamma}$ and IL-$1{\beta}$-induced cell proliferation, released IL-6 level was measured. $IFNP{\gamma}$ and IL-$1{\beta}$ cause an increase of released IL-6 protein level in a time-dependent manner. Furthermore, pretreatment with IL-6 antibody (0, 0.1, 1, 2.5, and 5 ng/ml) dose-dependently inhibited the $IFNP{\gamma}$ and IL-$1{\beta}$-induced cell proliferation. However, bezafibrate and fenofibrate did not affect increased mRNA and protein levels of IL-6 in $IFNP{\gamma}$ and IL-$1{\beta}$-stimulated astrocytes. Taken together, these results clearly suggest that activation of $PPAR{\alpha}$ attenuates the $IFNP{\gamma}$ and IL-$1{\beta}$-induced cell proliferation through IL-6 independent pathway.

The Effects of Coptis japonica Makino(CJM) Extract on the Alzheimer's Disease Model (일황련(日黃連)이 치과병태(痴果病態)모델에 미치는 영향(影響))

  • Jung, In-Chul;Lee, Sang-Ryong;Park, Ji-Un
    • Journal of Oriental Neuropsychiatry
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    • v.15 no.1
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    • pp.87-99
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    • 2004
  • This experiment was designed to investigate the effect of Coptis japonica Makino(CJM) on the Alzheimer's disease. The effects of CJM extract on $IL-1{\beta}$, IL-6, amyloid precursor proteins (APP), acetylcholinesterase(AChE), glial fibrillary acidic protein(GFAP) mRNA of PC-12 cell treated by $A{\beta}$ plus $rIL-1{\beta}$ and AChE activity of PC-12 cell lysate treated by $A{\beta}$ plus $rIL-1{\beta}$ and behavior of memory deficit rats induced by scopolamine and mice glucose, uric acid, AChE activity of memory deficit rats induced by scopolamine were investigated, respectively. The results were summarized as follows ; 1. CJM extract suppressed $IL-1{\beta}$, IL-6 mRNA in PC-12 cell treated by $A{\beta}$ plus $rIL-1{\beta}$ 2. CJM extract suppressed APP, AChE, GFAP mRNA in PC-12 cell treated by $A{\beta}$ plus $rIL-1{\beta}$ 3. CJM extract suppressed AChE activity in cell lysate of PC-12 cell treated by $A{\beta}$ plus $rIL-1{\beta}$ 4. CJM extract group showed significantly inhibitory effect on the memory deficit of mice induced by scopolamine in the experiment of Morris water maze. 5. CJM extract increased glucose, decreased uric acid and AChE significantly in the serum of the memory deficit rats induced by scopolamine. According to the above results, it is suggested that CJM extract might be usefully applied for prevention and treatment of Alzheimer's disease and memory deficit symptom.

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Effects of Luteolin on IL-1β-Induced MCP1 Protein Expression (Luteolin의 IL-1β에 의한 MCP1 단백질 발현 증가에 미치는 영향)

  • Lim, Jun-Hee;Kwon, Taeg-Kyu
    • 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.

Triglycerides increase mRNA Expression of Pro-inflammatory Cytokines Via the iNOS in Jurkat T lymphocyte and U937 Monocyte Cell Lines (Jurkat T 림프구와 U937 단핵구에서 중성지방 처리 시 iNOS를 통한 염증성 사이토카인의 mRNA 발현 증가)

  • Chang, Jeong Hyun
    • Journal of the Korean Society of Radiology
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    • v.13 no.1
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    • pp.133-140
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    • 2019
  • Triglycerides (TG) are one of the triggers of chronic inflammatory lesions in the blood vessels. In the key factors in the development of inflammatory diseases, Pro-inflammatory cytokines such as tumor necrosis factor-alpha $(TNF-){\alpha}$ and interleukin-1 beta ($IL-1{\beta}$) contribute to the development of inflammatory lesions by recruiting other immune cells in the inflamed area or causing cell necrotic death. In this study, I investigated the effect of Jurkat T lymphocytes and U937 monocytes involved in vascular inflammation development on the expression of $TNF-{\alpha}$ and $IL-1{\beta}$ on exposure to TGs. In Jurkat cells, mRNA expression of $TNF-{\alpha}$ is increased by exposure to TGs. However, the expression levels of $TNF-{\alpha}$ and $IL-1{\beta}$ were increased by TGs in U937 cells. To investigate whether inducible nitric oxide synthase (iNOS) is involved in the increase of expression of $TNF-{\alpha}$ and $IL-1{\beta}$ by TGs, treatment of W1400 (an iNOS inhibitor) resulted in recovery of expression level both $TNF-{\alpha}$ and $IL-1{\beta}$. Based on the present study, it was confirmed that the expression of $TNF-{\alpha}$ and $IL-1{\beta}$ in monocytes and T lymphocytes. This increased cytokines contribute to development of vascular inflammatory lesions. In addition, iNOS is involved in the increase of $TNF-{\alpha}$ and $IL-1{\beta}$ expression by TGs.

Effects of Acupuncture and Radix Astragali Aqua-acupuncture on Transcriptional Expression of Mouse Cytokines $IL-1{\beta}$ (현유혈의 침자극과 황기약침이 실험용 생쥐의 면역활성물질 $IL-1{\beta}$의 유전자 발현에 미치는 영향)

  • 손수곤;김종수;박원환
    • The Journal of Korean Medicine
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    • v.21 no.4
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    • pp.16-25
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    • 2000
  • Objective : Acupuncture and Radix Astragali aqua-acupuncture stimuli have long been used to cure human diseases. However, the exact physiological and biochemical mechanisms involved remain undiscovered. Thus, many attempts have been made to show the scientific mechanisms involved. The effects of acupuncture and Radix Astragali aqua-acupuncture, which was known to date, as follow; effective circulation of body blood system and proliferation of leucocytes. Methods : In this study, we have applied acupuncture and Radix Astragali aqua-acupuncture stimuli to mouse on Sinsuhyul, a stimulative point of oriental medicine, to see effects on the expression of cytokine $IL-1{\beta}$. Mice were treated with lipopolysaccharide(LPS) for inflammation induction and then reverse transcriptase-polymerase chain reaction (RT-PCR) using each primer set were performed to trace the amounts of mRNA. Results : 1. $IL-1{\beta}$ was not expressed in LPS-nontreated mice at 15 to 60 min after acupuncture-stimuli. However, expression occurred after 3hrs. 2. $IL-1{\beta}$ was specifically expressed in LPS-treated mice at 30 min after acupuncture-stimuli. 3. $IL-1{\beta}$ was expressed in LPS-nontreated mice at 30 min after Radix Astragali aqua-acupuncture stimuli, however, not expressed at 60, 180 min. 4. $IL-1{\beta}$ was gradually expressed in LPS-treated mice at 15 to 180 min after Radix Astragali aqua-acupuncture stimuli. Conclusions : $IL-1{\beta}$ in LPS-treated mice was more effective than that of LPS-nontreated mice. We are now in the process of elucidating the immunological action mechanism of acupuncture and Radix Astragali aqua-acupuncture stimuli. And cytokine $IL-1{\beta}$ can be used not only as a basis of the effects of acupuncture and Radix Astragali aqua-acupuncture but also as a diagnosis guide through the immunological actions of those.

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Effects of Samjunghwan on the $IL-1{\beta}$ Gene Expression in the Macrophage (삼정환(三精丸)이 대식세포의 면역반응에서 유도되는 $IL-1{\beta}$ 유전자의 발현에 미치는 영향)

  • Kim, Se-Yoon;Jeong, Ji-Cheon
    • The Journal of Internal Korean Medicine
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    • v.27 no.1
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    • pp.228-236
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    • 2006
  • Objectives : Macrophage has an important innate defense role in the immune system. When we are infected with pathogens, macrophage ingests them through phagocytosis or endocytosis, and then secretes many cytokines, such as IL-1, IL-6 and $TGF{\alpha}$, which are regulators of immune responses. The aim of this study is to determine how Samjunghwan effects the expression of cytokine and other immune-related genes in macrophages. Methods : Cells were treated directly with Samjunghwan and/or LPS at regular intervals. Total RNA of cells was isolated using TRIzol reagent, and the changes in cytokine gene expressions were investigated using RT-PCR, western blot and ELISA. Results : $IL-1{\alpha},\;IL-1{\beta}$ and COX-2 genes were inducibly expressed specifically by Samjunghwan in macrophage. Especially, $IL-1{\beta}$ gene was induced most strongly by treatment with Samjunghwan. Over time, treatment with Samjunghwan showed that the expression levels of $IL-1{\alpha}\;and\;$IL-1{\beta}$ genes increased from 1 to 4h, and then decreased from 4 to ISh. However, the expression level of COX-2 gene increased continuously up to 11h. $IL-1{\alpha},\;IL-1{\beta}$ and COX-2 genes were expressed synergistically by a simultaneous treatment of both Samjunghwan and LPS in macrophages. Secretion levels of translated $IL-1{\beta}$ increased continuously up to 11h. Conclusions : Though this study is only a start in the investigation of the efficasy of Samjunghwan, these results suggest that Samjunghwan has positive effects on immune responses.

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A Study on Anti-Bone Resorption & Osteoporosis by Taeyoungion-Jahage Extracts

  • Bae, Hyo-Sang;Cho, Hyung-Lae;Kim, Dong-Il;Lee, Tae-Kyun;Kim, Jun-Ki;Shin, Jung-Sik
    • The Journal of Korean Obstetrics and Gynecology
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    • v.15 no.4
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    • pp.61-75
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    • 2002
  • Recombinant human $interleukin-1{\beta}$ $(rhIL-1{\beta})$ regulates several activities of the osteoblast cells derived from mouse calvarial bone explants in vitro. $rhIL-1{\beta}$ stimulated cellular proliferation and the synthesis of prostaglandin $E_2(PGE_2)$ and plasminogen activator activity in the cultured cells in a dose-dependent manner. However, the induction of osteocalcin synthesis and alkaine phosphatase activity in response to vitamine D, two characteristics of the osteoblast phenotype, were antagonized by $rhIL-1{\beta}$ over a similar dose range. This study supports the role of $IL-1{\beta}$ in the pathological modulation of bone cell metabolism, with regard to implication in the pathogenesis of osteoporosis by $IL-1{\beta}$. When the mouse calvarial bone cells were used, the bone resorption induced by $IL-1{\beta}$ was strongly inhibited by calcitonin treatment, indicating osteoclast-mediated bone resorption. On the other hand, the medicinal extracts of Taeyoungjon-Jahage (T.Y.J-J.H.G extracts) was tested for whether they could inhibit $IL-1{\beta}-induced$ $PGE_2$ production. Cell viability was not significantly affected by treatment with the indicated concentration of the extracts. The T.Y.J.-J.H.G. extracts were shown to have the inhibitory effects against the synthesis of $PGE_2$. We also examined the effect of the pretreatment with a various concentrations of the T.Y.J.-J.H.G. extracts then treated the $PGE_2-induction$ agents. Pretreatment of the T.Y.J.-J.H.G. extracts for 1 h, which by itself had little effect on cell survival, did not enhance the synthesis of $PGE_2$. Furthermore, the T.Y.J-J.H.G. extracts were shown to have the protective effects against plasminogen dependent fibrinolysis induced by the bone resorption agents of $IL-1{\beta}$. Pretreatment of the T.Y.J.-J.H.G. extracts for 1 h did not enhance the plasminogen dependent fibrinolysis. Finally, calcitonin showed the inhibitory activity the $IL-1{\beta}-stimulated$ bone resorption in the mouse calvarial bone cells having both of the osteoblast and osteoclast cells. Seemingly, pretreatment of the T.Y.J.-J.H.G. extracts for 1 h reduced the bone resorption. These results clearly indicated that calcitonin and T.Y.J.-J.H.G. extracts play key roles in inhibition of the osteoclast-mediated bone resorption.

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The Relationship Between Interleukin $1{\beta}$ Gene Polymorphism and Renal Involvement in Henoch-$Sch\ddot{o}nlein$ Purpura (Henoch-$Sch\ddot{o}nlein$ Purpura에서 Interleukin $1{\beta}$ 유전자 다형성과 신장 침범과의 연관성)

  • Na, Hyoung-Joon;Go, Il-Yong;Yoon, Joon-Ho;Yeh, Byung-Il;Kim, Hwang-Min
    • Childhood Kidney Diseases
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    • v.10 no.2
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    • pp.125-131
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    • 2006
  • Purpose : High interleukin-1 beta(IL-$1{\beta}$) expression in the skin biopsy specimens of patients with Henoch-$Sch\ddot{o}nlein$ Purpura(HSP) has been observed. We examined IL-$1{\beta}$ gene polymorphism in patients with HSP. The purpose of this study is to examine the relationship between IL-$1{\beta}$ gene polymorphism and renal involvement in HSP. Methods : Patients from mideast Korea with HSP were studied. All patients had at least 6 months of follow up. Patients and ethnically matched controls were genotyped for IL-$1{\beta}$ gene polymorphism by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP). Results : Thirty-four patients(all younger than 15 years old) who had been diagnosed with HSP and 27 controls were examined. No allele or genotype differences between the HSP and control groups were observed. No significant association between the carriage of IL-$1{\beta}$(-511) T allele and renal involvement(P=0.525, OR:1.417, CI:0.545-3.686) was found. Conclusion : In unselected patients with HSP, carriage of IL-$1{\beta}$(-511) T allele does not appear to influence renal involvement.

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Effects of Sungsimjihwang-tang Hot Water Extract & Ultra-fine Powder on the Alzheimer's Disease Model (성심지황탕(醒心地黃湯) 열수추출물과 초미세분말제형이 Alzheimer's Disease 병태 모델에 미치는 영향)

  • Min, Kyung-Jik;Lee, Sang-Ryong;Jung, In-Chul
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.22 no.5
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    • pp.1178-1191
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    • 2008
  • This experiment was designed to investigate the effect of the SSJHT hot water extract & ultra-fine Powder on Alzheimer's Disease Model Induced by ${\beta}A$. The effects of the SSJHT hot water extract on expression of IL-1RA, $IL-1{\beta}$$, IL-6, IL-10, $TNF-{\alpha}$, NOS-II, COX-2 mRNA and production of $IL-1{\beta}$, IL-6, $TNF-{\alpha}$ in BV2 microglial cell line treated by lipopolysacchaide(LPS). The effects of the SSJHT hot water extract & ultra-fine powder on (1) the behavior (2) expression of $IL-1{\beta}$, $TNF-{\alpha}$, MDA, CD68, CD11b and AChE (3) and the infarction area of the hippocampus in Alzheimer's diseased mice induced with ${\beta}A$ were investigated. The SSJHT hot water extract suppressed the expression of $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$, NOS-II, COX-2 mRNA and increased IL-1RA, IL-10 in BV2 microglia cell line treated with LPS. The SSJHT hot water extract suppressed the production of $IL-1{\beta}$, IL-6, $TNF-{\alpha}$ significantly in BV2 microglial cell line treated with LPS. The SSJHT hot water extract & ultra-fine powder a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by ${\beta}A$ in the Morris water maze experiment, which measured step-through latency. The SSJHT hot water extract & ultra-fine powder suppressed the expression of $TNF-{\alpha}$$, $L-1{\beta}$ protein significantly in the microglial cell of mice with Alzheimer's disease induced by ${\beta}A$. The SSJHT hot water extract & ultra-fine powder reduced the MDA and suppressed the over-expression of CD68, CD11b in the mice with Alzheimer's disease induced by ${\beta}A$. The SSJHT hot water extract & ultra-fine powder significantly decreased AChE activity in the serum of the mice with Alzheimer's disease induced by ${\beta}A$. The SSJHT hot water extract & ultra-fine powder reduced infarction area of hippocampus. and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}A$. The results suggest that the SSJHT hot water extract & ultra-fine powder may be effective for treatment of Alzheimer's disease. Investigation into the clinical use of the SSJHT hot water extract & ultra-fine powder for Alzheimer's disease is suggested for future research.

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.