• Title/Summary/Keyword: Interleukin-$1{\alpha}$

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Effects of Poncirus trifoliata Pharmacopuncture on plasma lipid composition and concentration of $TNF-{\alpha}$ and IL-6 in rats fed high fat diet (지각(枳穀) 약침이 고지방 식이 급여 흰쥐의 혈액 내 지질구성과 $TNF-{\alpha}$ 및 IL-6농도에 미치는 영향)

  • Lee, Jong-Wook;Lee, Ji-Hyang;Lee, Eun;Lee, Joon-Moo
    • Korean Journal of Acupuncture
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    • v.23 no.1
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    • pp.37-44
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    • 2006
  • Objective : To investigate the effects of Poncirus trifoliata Pharmacopuncture on lowering lipid and contents of serum tumor necrosis $factor-{\alpha}$ $(TNF-{\alpha})$ and interleukin-6 (IL-6) in hyperlipidemic rats. Methods : Triglyceride, total cholesterol, $TNF-{\alpha}$, and IL-6 levels in Poncirus trifoliata Pharmacopuncture groups were compared with those in the control group. Results : Concentration of triglyceride and total cholesterol in plasma was decreased in the Poncirus trifoliata Pharmacopuncture groups. In Poncirus trifoliata Pharmacopuncre groups, plasma LDL-cholesterol showed a lower value and HDL-cholesterol showed a higher value than those of the control group. Contents of $TNF-{\alpha}$ was decreased in the Poncirus trifoliata Pharmacopuncture groups. Contents of IL-6, however, were not significantly different. Conclusions : The results suggest that Poncirus trifoliata Pharmacopuncture may have an impact on lipid metabolism to potentially prevent development of diabetes mellitus and accompanying cerebrovascular diseases.

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Studies on Anti-inflammatory Effects of Yangdan-tang Extracts (양단탕 추출물의 항염증 효과에 대한 연구)

  • Choi, Su Ryeon;Hwang, Hyung Seo;Kim, Tae Yeon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.34 no.5
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    • pp.238-244
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    • 2020
  • Yangdan-tang (YD) is recorded as a treatment to treat exterior-related fever illness in the Korean medicine. In this study, we examined the anti-inflammatory effects of YD, using YD water extract and lipopolysaccharide (LPS)-induced RAW 264.7 cells. First of all, we measured the amount of nitric oxide (NO) and prostaglandin E2 (PGE2), the products of inflammatory metabolism. Also, we measured enzymes such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as cytokines such as tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), interleukin 1 alpha (IL-1α), and interleukin 1 beta (IL-1β). YD suppressed the production of NO and PGE2 in a dose dependent manner and reduced the amount of protein and the mRNA expression of iNOS and COX-2. Also, YD reduced the mRNA expression of TNF-α, IL-6, IL-1α and IL-1β. In conclusion, YD decreased production of LPS-induced inflammatory factor, which could be a clinical basic subject for inflammatory diseases.

Regulation of Cytokine Production by Exogenous Nitric oxide in Murine Splenocyte and Peritoneal Macrophage

  • Eun, Jae-Soon;Suh, Yong-Hoon;Kim, Dae-Keun;Jeon, Hoon
    • Archives of Pharmacal Research
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    • v.23 no.5
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    • pp.531-534
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    • 2000
  • Nitric oxide (NO), products of activated macrophages, have a great impact on the regulation of cytokine production. The role of NO in non-specific host cells is commonly accepted. On the contrary, its role as an immuno-regulatory molecule is still controversial. In this study, we have investigated the effect of NO on the production of cytokines from murine splenocytes and macrophages. S-nitroso-L-glutathione inhibited the release of both interferone-$\gamma$ and interleukin-2 produced by Th1 cells and tumor necrosis factor-$\alpha$ and interleukin-1$\beta$ produced by macrophages, but did not affect the release of interleukin-4 and interleukin-10 produced by Th2 cells. These results suggest that NO exerts a down-regulatory effect on the secretion of cytokines from Th1 cells and macrophages which are implicated in immune response. Thus, NO may have an important role as an immune-modulatory as well as effector molecule in the immune system.

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Generation of Antagonistic RNA Aptamers Specific to Proinflammatory Cytokine Interleukin-32

  • Kim, Se-Ho;Kim, Jung-Hee;Yoon, Su-Jin;Kim, Keun-Sik;Yoon, Moon-Young;Yoon, Do-Young;Kim, Dong-Eun
    • Bulletin of the Korean Chemical Society
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    • v.31 no.12
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    • pp.3561-3566
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    • 2010
  • Interleukin 32 (IL-32) is a recently identified cytokine that induces major proinflammatory cytokines such as $TNF{\alpha}$ and IL-$1{\beta}$, which play an important role in chronic inflammatory diseases. To antagonize the biological function of IL-32 in cells, we generated RNA aptamers that could bind specifically to IL-32 protein. The highest affinity aptamer, AC3-3, successfully antagonized IL-32 by abolishing the induction of $TNF{\alpha}$ in the human lung carcinoma cells expressing IL-32. This aptamer could be used as a potent and selective antagonist against IL-32 to further elucidate the roles of IL-32 in chronic inflammatory diseases, as well as a therapeutic agent.

FSL-1, a Toll-like Receptor 2/6 Agonist, Induces Expression of Interleukin-$1{\alpha}$ in the Presence of 27-hydroxycholesterol

  • Heo, Weon;Kim, Sun-Mi;Eo, Seong-Kug;Rhim, Byung-Yong;Kim, Koanhoi
    • The Korean Journal of Physiology and Pharmacology
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    • v.18 no.6
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    • pp.475-480
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    • 2014
  • We investigated the question of whether cholesterol catabolite can influence expression of inflammatory cytokines via Toll-like receptors (TLR) in monocytic cells. Treatment of THP-1 monocytic cells with 27-hydroxycholesterol (27OHChol) resulted in induction of gene transcription of TLR6 and elevated level of cell surface TLR6. Addition of FSL-1, a TLR6 agonist, to 27OHChol-treated cells resulted in transcription of the $IL-1{\alpha}$ gene and enhanced secretion of the corresponding gene product. However, cholesterol did not affect TLR6 expression, and addition of FSL-1 to cholesterol-treated cells did not induce expression of $IL-1{\alpha}$. Using pharmacological inhibitors, we investigated molecular mechanisms underlying the expression of TLR6 and $IL-1{\alpha}$. Treatment with Akt inhibitor IV or U0126 resulted in significantly attenuated expression of TLR6 and $IL-1{\alpha}$ induced by 27OHChol and 27OHChol plus FSL-1, respectively. In addition, treatment with LY294002, SB202190, or SP600125 resulted in significantly attenuated secretion of $IL-1{\alpha}$. These results indicate that 27OHChol can induce inflammation by augmentation of TLR6-mediated production of $IL-1{\alpha}$ in monocytic cells via multiple signaling pathways.

Effects of Prunella vulgaris Pharmacopuncture on Lipopolysaccharide-Induced Acute Inflammatory Rat Model (하고초 약침이 LPS로 유발된 급성염증 백서 모델에 미치는 영향)

  • Lee, Jong-Wook;Lee, Hyang-Sook;Lee, Eun;Lee, Joon-Moo
    • Korean Journal of Acupuncture
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    • v.26 no.3
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    • pp.43-54
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    • 2009
  • Objectives : To investigate the anti-inflammatory effects of Prunella vulgaris pharmacopuncture in lipopolysaccharide (LPS)-induced inflammatory rat model. Methods : Sprague-Dawley rats were divided into 5 groups; normal control (n=8), LPS control (n=8), LPS+Prunella vulgaris pharmacopuncture at CV4 (CV4, n=8), LPS+Prunella vulgaris pharmacopuncture at ST36 (ST36, n=8), and LPS+Prunella vulgaris pharmacopuncture at CV12 (CV12, n=8). Pharmacopuncture was given every two days for 4 weeks followed by inflammation induction by peritoneal LPS injection (5mg/kg). Proinflammatory cytokines including interleukin-$1{\beta}$ (IL-$1{\beta}$), interleukin-6 (IL-6), tumor necrosis factor-$\alpha$ (TNF-$\alpha$), interleukin-10 (IL-10), thiobarbituric acid reactive substance (TBARS) from blood and liver tissue were compared before and 5 hrs after inflammation induction. Results : In CV4 and CV12 groups, plasma IL-$1{\beta}$, IL-6 and TNF-$\alpha$ levels increased by LPS injection, significantly decreased 5 hrs after injection (p<0.05). For CV12 group, plasma IL-10 concentration significantly increased (p<0.05). Liver IL-$1{\beta}$ and IL-6 levles significantly decreased in CV4 and CV12 groups (P<0.05), while normal and LPS control groups were not significantly different in TNF-$\alpha$ and IL-10 levels. Plasma TBARS concentration was significantly decreased in CV12 group, while there was no significant difference among LPS control and pharmacopuncture groups for liver TBARS concentration. Conclusions : Based on the present findings, Prunella vulgaris pharmacopuncture at CV12 may have a potentially preventive anti-inflammatory effect in an LPS-induced inflammatory rat model.

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Association of Intracellular $T_H1-T_H2$ Balance in CD4+ T-cells and MIP-$1{\alpha}$ in CD8+ T-cells with Disease Severity in Adults with Dengue

  • Kadhiravan, Tamilarasu;Saxena, Ankit;Singh, Amar;Broor, Shobha;Sharma, Surendra K.;Mitra, Dipendra K.
    • IMMUNE NETWORK
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    • v.10 no.5
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    • pp.164-172
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    • 2010
  • Background: We tested the hypothesis that dengue haemorrhagic fever (DHF) is associated with a $T_H1$-skewed immune response as opposed to dengue fever (DF). Methods: We estimated intracellular (in T-cells) and serum levels of designate $T_H1/T_H2$ cytokines [interferon-${\gamma}$ (IFN-${\gamma}$), interleukin-4 (IL-4), and tumor necrosis factor-${\alpha}$] and macrophage inflammatory protein-$1{\alpha}$ (MIP-$1{\alpha}$) at admission, 48h, and day 5 in 20 adults with dengue (DF=10, DHF=10) and 10 dengue-naive healthy controls. Results: At admission, intracellular IFN-${\gamma}$/IL-4 ratio in CD4+ T-cells and proportion of MIP-$1{\alpha}$-positive CD8+ T-cells were significantly higher in patients with DHF [7.21 (5.36~10.81) vs. 3.04 (1.75~4.02); p=0.011 and 6.2% (3.2~8.2%) vs. 2.4% (2.0~3.6%); p=0.023]. The latter showed a significant positive correlation with IFN-${\gamma}$/IL-4 ratio in CD4+ T-cells (Spearman's rho=0.64; p=0.003), percentage-change in haematocrit (rho=0.47; p=0.048), and serum alanine amino-transferase level (rho=0.61; p=0.009). Conclusion: We conclude that DHF is associated with a $T_H1$-skewed immune response. Further, MIP-$1{\alpha}$ in CD8+ T-cells is an important immunologic correlate of disease severity in dengue.

The Experimental study of Hwagae-san on Anti-Inflammatory Effect (화개산(華蓋散)의 항염에 대한 실험적 연구)

  • No, Woon-Serb;Shin, Jo-Young;Lee, Si-Hyeong
    • Herbal Formula Science
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    • v.16 no.2
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    • pp.101-114
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    • 2008
  • Objective : The purpose of this study was to investigate the anti-inflammatory effects of Hwagae-san extract(HGSE) on the peritoneal macrophage. Methods : To evaluate anti-inflammatory effects of HGSE, We measured cytokines(interleukin-6; IL-6, interleukin-12; IL-12, tumor necrosis factor-${\alpha}$; TNF-${\alpha}$) and nitric oxide(NO) production in lipopolysaccharide(LPS)-induced macrophages. Furthermore, We examined molecular mechanism using western blot and also LPS-induced endotoxin shock. Results : 1. HGSE did not have any cytotoxic effect in the peritoneal macrophages. 2. HGSE reduced LPS-induced IL-6, TNF-${\alpha}$, IL-12 and NO production in peritoneal macrophages. 3. HGSE inhibited the activation of extracelluar signal-regulated kinase(ERK), C-Jun NH2-terminal kinase(JNK) but not of p38, degradation of IkB-${\alpha}$ in the LPS-stimulated peritoneal macrophages. 4. HGSE inhibited the production of TNF-$\alpha$, IL-6 and IL-12 in serum after LPS injection. Conclusion : These results suggest that HGSE may inhibit the production of TNF-${\alpha}$, IL-6, and IL-12 through inhibition of ERK and JNK activation, and that HGSE may be beneficial for inflammatory diseases.

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IL-1 Receptor Antagonist Reduced Chemical-Induced Keratinocyte Apoptosis through Antagonism to IL-1α/IL-1β

  • Lee, Hyejin;Cheong, Kyung Ah;Kim, Ji-Young;Kim, Nan-Hyung;Noh, Minsoo;Lee, Ai-Young
    • Biomolecules & Therapeutics
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    • v.26 no.4
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    • pp.417-423
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    • 2018
  • Extracellular interleukin 1 alpha (IL-$1{\alpha}$) released from keratinocytes is one of the endpoints for in vitro assessments of skin irritancy. Although cells dying via primary skin irritation undergo apoptosis as well as necrosis, IL-$1{\alpha}$ is not released in apoptotic cells. On the other hand, active secretion has been identified in interleukin-1 receptor antagonist (IL-1ra), which was discovered to be a common, upregulated, differentially-expressed gene in a microarray analysis performed with keratinocytes treated using cytotoxic doses of chemicals. This study examined whether and how IL-1ra, particularly extracellularly released IL-1ra, was involved in chemically-induced keratinocyte cytotoxicity and skin irritation. Primary cultured normal adult skin keratinocytes were treated with cytotoxic doses of chemicals (hydroquinone, retinoic acid, sodium lauryl sulfate, or urshiol) with or without recombinant IL-1ra treatment. Mouse skin was administered irritant concentrations of hydroquinone or retinoic acid. IL-1ra (mRNA and/or intracellular/extracellularly released protein) levels increased in the chemically treated cultured keratinocytes with IL-$1{\alpha}$ and IL-$1{\beta}$ mRNAs and in the chemically exposed epidermis of the mouse skin. Recombinant IL-1ra treatment significantly reduced the chemically-induced apoptotic death and intracellular/extracellularly released IL-$1{\alpha}$ and IL-$1{\beta}$ in keratinocytes. Collectively, extracellular IL-1ra released from keratinocytes could be a compensatory mechanism to reduce the chemically-induced keratinocyte apoptosis by antagonism to IL-$1{\alpha}$ and IL-$1{\beta}$, suggesting potential applications to predict skin irritation.

Morphological Study of Acute Lung Injury Induced by Interleukin-1$\alpha$ Intratracheally in Young and Old Rats (젊은 흰쥐와 늙은 흰쥐에서 인터루킨-1$\alpha$로 유도된 급성폐손상에 관한 형태학적 연구)

  • 조현국;이영만;박원학
    • Biomedical Science Letters
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    • v.3 no.2
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    • pp.139-150
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    • 1997
  • In order to investigate the effect of aging and the $H_2O$$_2$ localization in association with histological, ultrastructural, and cytochemical studies in lung tissue after interleukin-1$\alpha$(IL-1) induced lung injury, an acute lung injury was induced by instillation of IL-1 into the trachea. Both of 4- and 20-months-old male rats, protein contents in IL-1 treated branchoalveolar lavage increased significantly compared to each control rats. Acute lung injury occured by oxidative stress because neutrophils accumulated in vascular lumen and formed the adhesion with endothelial cells. As these cause, tissue proteins were exuded and leukocytes migrated into the alveolar lumen. Neverthless in these lung injury $H_2O$$_2$ localization of IL-1 treated 20 months rats was not different compared to IL-1 treated 4 months rats. After all aging was not a factor to accelate IL-1 induced lung injury. Based on these results, it is suggested that neutrophil infilteration might be an important cause in acute lung injury, and aging is not a factor to change the acute lung injury by oxidative stress.

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