• Title/Summary/Keyword: Proinflammatory cytokines

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Pandanus amaryllifoius Roxb. Leaves Ethanol Extract Ameliorates Lipid and Proinflammatory Cytokines Profiles in a Rat Model of Dyslipidemia

  • Martohap Parotua Lumbanraja;Kusnandar Anggadiredja;Neng Fisheri Kurniati;Hubbi Nashrullah Muhammad
    • Journal of Pharmacopuncture
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    • v.27 no.2
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    • pp.101-109
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    • 2024
  • Objectives: Dyslipidemia has currently become a major health challenge that still opens for safer and more effective modes of treatment. The plant Pandanus amaryllifolius Roxb. (pandan) has been indicated to contain active ingredients that interfere with the pathological pathway of dyslipidemia. The aim of the study was to test the effects of pandan leaves ethanol extract on lipid and proinflammatory profiles in a rat dyslipidemic model. Methods: Dyslipidemia was induced by administration of high-fat feed for 8 weeks. Treatments (vehicle, the reference drug simvastatin at 1.8 mg/kg, and extract at 200, 300 or 600 mg/kg) were given for 4 weeks following the completion of induction. Results: Significant post-treatment decreases in total cholesterol, low density lipoprotein (LDL), and triglyceride levels in groups receiving all doses of extract and simvastatin were observed. Similar results were also found in regards to proinflammatory cytokines levels. Pandan extracts significantly lowered the concentrations of IL-6, TNF-α, and NFκB p65. Characterization of metabolite contents of the extract confirmed the presence of the previously suggested active alkaloids pandamarilactonine-A and B. Conclusion: Taken together, results of the present study implied the ameliorating effects of pandan leaves ethanol extract in dyslipidemic condition which is potential for opening an avenue in combating this essential component of metabolic disorder.

Anticancer and Anti-Inflammatory Activity of Probiotic Lactococcus lactis NK34

  • Han, Kyoung Jun;Lee, Na-Kyoung;Park, Hoon;Paik, Hyun-Dong
    • Journal of Microbiology and Biotechnology
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    • v.25 no.10
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    • pp.1697-1701
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    • 2015
  • The anticancer and anti-inflammatory activities of probiotic Lactococcus lactis NK34 were demonstrated. Treatment of cancer cells such as SK-MES-1, DLD-1, HT-29, LoVo, AGS, and MCF-7 cells with 106 CFU/well of L. lactis NK34 resulted in strong inhibition of proliferation (>77% cytotoxicity, p < 0.05). The anti-inflammatory activity of L. lactis NK34 was also demonstrated in lipopolysaccharide-induced RAW 264.7 cells, where the production of nitric oxide and proinflammatory cytokines (tumor necrosis factor-α, interleukin-18, and cyclooxygenase-2) was reduced. These results suggest that L. lactis NK34 could be used as a probiotic microorganism to inhibit the proliferation of cancer cells and production of proinflammatory cytokines.

Anti-inflammatory Activities of Cheongpyehwadam-tang

  • Kwak Sang-Ho;Kim Ji-Young;Han Eun-Hee;Oh Kyo-Nyeo;Kim Dong-Hee;Jeong Hye-Gwang;Yoo Dong-Youl
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.19 no.5
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    • pp.1399-1404
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    • 2005
  • In oriental medicine, Cheongpyehwadam-tang (CHT) has long been used for the cure of inflammatory diseases in the lung and bronchus such as bronchitis, bronchial asthma, pneumonia and tuberculosis. It's use is currently further extended for the treatment of allergic asthma. To investigate the anti-inflammatory effects of CHT, we investigated the effects of CHT on the lipopolysaccharide (LPS)-induced nitric oxide (NO) and pro-inflammatory cytokines ($TNF-{\alpha}$, IL-6, and $IL-1{\beta}$) production, and on the level of inducible nitric oxide synthase (iNOS) and proinflammatory cytokines expression in murine macrophage RAW 264.7 cells. CHT alone did not affect NO or pro-inflammatory cytokines production. In contrast, CHT inhibited LPS-induced NO and proinflammatory cytokines and the levels of LPS-induced iNOS and proinflarnmatory cytokine mRNA in a dose-dependent manner. CHT also inhibited the nuclear factor-kappa B (NF-kB) activation. Taken together, these results suggested that CHT inhibits the production of NO and pro-inflammatory cytokines in RAW 264.7 cells through blockade of NF-kB activation.

Effects of Zinc Chloride on the Lipopolysaccharide-induced Production of Cytokines in Tumor-bearing Mice (암유발생쥐에 리포폴리사카라이드에 의해 유도된 사이토카인의 생산에 미치는 염화아연의 영향)

  • 채병숙
    • YAKHAK HOEJI
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    • v.45 no.5
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    • pp.557-564
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    • 2001
  • To determine effects of zinc on lipopolysaccharide (LPS)-induced production of proinflammatory cytokines and Iymphokines in tumor-bearing ICR mice, this study has been investigated. Zinc chloride (Zn) at doses of 1 mg/kg was administered orally 30 minutes before i.p. injection of LPS (8 mg/kg) 5 times for 7 days. LPS greatly increased tumor necrosis factor (TNF)-$\alpha$ and interleukin (IL)-1$\beta$, in both serum and splenic supernatants compared with those in controls. However Zn strongly decreased LPS-increased production of TNF-$\alpha$ and IL-1$\beta$ in spleenic supernatants compared with those in controls and insignificantly also reduced in serum. LPS insignificantly decreased IL-2 levels in spleenic supernatants compared with those in controls but significantly increased interferon (IFN)-${\gamma}$ levels. Zn didn't affect IL-2 production in splenic supernatants compared to controls but significantly enhanced the LPS-decreased production of IL-2. Zn significantly increased IFN-${\gamma}$ levels in splenic supernatants compared to controls and did not affect the LPS-increased production of IFN-${\gamma}$. These findings suggest that Zn may strongly attenuate the LPS-induced pathogenesis of proinflammatory cytokines in tumor-bearing state and significantly up-regulate the LPS-induced function of T cells to produce IL-2 with maintaining normally the LPS- increased levels of IFN-${\gamma}$.

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Pro-inflammatory Cytokine Production Inhibitory Effects of Frankincence in Murine Macrophage (마우스의 대식세포에서 프랑킨센스의 염증성 사이토카인 분비 억제작용)

  • Park, Jeong-Sook
    • Journal of the Korea Convergence Society
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    • v.8 no.1
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    • pp.239-243
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    • 2017
  • This study aims to demonstrate the inhibitory effect of proinflammatory cytokines by using Frankinsense. The present data was designed to determine the production of the frankincence on pro-inflammatory factors such as $TNF-{\alpha}$ and $IL-1{\beta}$ in lipopolysaccharide(LPS) stimulated RAW264.7 macrophages cell. The cell toxicity was identified by CellTiter 96 AQueous One solution cell proliferation assay. To evaluate of anti-inflammatory effect of frankincence, pro-inflammatory cytokines were measured by ELISA kit. As a result, the frankincence reduced NO and $TNF-{\alpha}$ production without cytotoxicity. As a result, Francincense was not cytotoxic at 10 ug / ml-1000 ug / ml and significantly inhibited the proinflammatory cytokines $TNF-{\alpha}$ and $IL-1{\beta}$. The secretion inhibition effect of proinflammatory cytokine is believed to be applicable to various physiological activity data and functional materials to demonstrate the anti - inflammatory properties of frankincense.

S100A4 Gene is Crucial for Methionine-Choline-Deficient Diet-Induced Non-Alcoholic Fatty Liver Disease in Mice

  • Zhang, Yin-Hua;Ma, De-Qiang;Ding, De-Ping;Li, Juan;Chen, Lin-Li;Ao, Kang-Jian;Tian, You-You
    • Yonsei Medical Journal
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    • v.59 no.9
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    • pp.1064-1071
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    • 2018
  • Purpose: To explore the influence of S100 calcium binding protein A4 (S100A4) knockout (KO) on methionine-choline-deficient (MCD) diet-induced non-alcoholic fatty liver disease (NAFLD) in mice. Materials and Methods: S100A4 KO mice (n=20) and their wild-type (WT) counterparts (n=20) were randomly divided into KO/MCD, Ko/methionine-choline-sufficient (MCS), WT/MCD, and WT/MCS groups. After 8 weeks of feeding, blood lipid and liver function-related indexes were measured. HE, Oil Red O, and Masson stainings were used to observe the changes of liver histopathology. Additionally, expressions of S100A4 and proinflammatory and profibrogenic cytokines were detected by qRT-PCR and Western blot, while hepatocyte apoptosis was revealed by TUNEL staining. Results: Serum levels of aminotransferase, aspartate aminotransferase, triglyceride, and total cholesterol in mice were increased after 8-week MCD feeding, and hepatocytes performed varying balloon-like changes with increased inflammatory cell infiltration and collagen fibers; however, these effects were improved in mice of KO/MCD group. Meanwhile, total NAFLD activity scores and fibrosis were lower compared to WT+MCD group. Compared to WT/MCS group, S100A4 expression in liver tissue of WT/MCD group was enhanced. The expression of proinflammatory ($TGF-{\alpha}$, $IL-1{\beta}$, IL-6) and profibrogenic cytokines ($TGF-{\beta}1$, COL1A1, ${\alpha}-SMA$) in MCD-induced NAFLD mice were increased, as well as apoptotic index (AI). For MCD group, the expressions of proinflammatory and profibrogenic cytokines and AI in KO mice were lower than those of WT mice. Conclusion: S100A4 was detected to be upregulated in NAFLD, while S100A4 KO alleviated liver fibrosis and inflammation, in addition to inhibiting hepatocyte apoptosis.

Korean Red Ginseng improves atopic dermatitis-like skin lesions by suppressing expression of proinflammatory cytokines and chemokines in vivo and in vitro

  • Kee, Ji-Ye;Jeon, Yong-Deok;Kim, Dae-Seung;Han, Yo-Han;Park, Jinbong;Youn, Dong-Hyun;Kim, Su-Jin;Ahn, Kwang Seok;Um, Jae-Young;Hong, Seung-Heon
    • Journal of Ginseng Research
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    • v.41 no.2
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    • pp.134-143
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    • 2017
  • Background: The prevalence of allergic inflammatory diseases such as atopic dermatitis (AD), asthma, and allergic rhinitis worldwide has increased and complete recovery is difficult. Korean Red Ginseng, which is the heat-processed root of Panax ginseng Meyer, is widely and frequently used as a traditional medicine in East Asia. In this study, we investigated whether Korean Red Ginseng water extract (RGE) regulates the expression of proinflammatory cytokines and chemokines via the mitogen-activated protein kinases (MAPKs)/nuclear factor kappa B ($NF-{\kappa}B$) pathway in allergic inflammation. Methods: Compound 48/80-induced anaphylactic shock and 1-fluoro-2,4-dinitrobenzene (DNFB)-induced AD-like skin lesion mice models were used to investigate the antiallergic effects of RGE. Human keratinocytes (HaCaT cells) and human mast cells (HMC-1) were also used to clarify the effects of RGE on the expression of proinflammatory cytokines and chemokines. Results: Anaphylactic shock and DNFB-induced AD-like skin lesions were attenuated by RGE administration through reduction of serum immunoglobulin E (IgE) and interleukin (IL)-6 levels in mouse models. RGE also reduced the production of proinflammatory cytokines including $IL-1{\beta}$, IL-6, and IL-8, and expression of chemokines such as IL-8, thymus and activation-regulated chemokine (TARC), and macrophage-derived chemokine (MDC) in HaCaT cells. Additionally, RGE decreased the release of tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), $IL-1{\beta}$, IL-6, and IL-8 as well as expressions of chemokines including macro-phage inflammatory protein $(MIP)-1{\alpha}$, $MIP-1{\beta}$, regulated on activation, normal T cell expressed and secreted (RANTES), monocyte chemoattractant protein (MCP)-1, and IL-8 in HMC-1 cells. Furthermore, our data demonstrated that these inhibitory effects occurred through blockage of the MAPK and $NF-{\kappa}B$ pathway. Conclusion: RGE may be a useful therapeutic agent for the treatment of allergic inflammatory diseases such as AD-like dermatitis.

Effect of Licochalcone A on the Production of Cytokines in LPS-Activated RAW264.7 Macrophage Cells (Licochalcone A가 대식세포주의 사이토카인 생성에 미치는 영향)

  • Lee, Gi-Sae;Lee, Sung-Ho;Cho, Young-Chang;Yoon, Goo;Cheon, Seung-Hoon;Kang, Bok-Yun
    • YAKHAK HOEJI
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    • v.53 no.6
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    • pp.321-327
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    • 2009
  • Licochalcone A is a chalcone isolated from the roots of Glycyrrhiza inflate. In this study, we examined the effects of licochalonce A on the production of cytokines in LPS-activated macrophages. Licochalcone A inhibited the secretion of proinflammatory cytokines such as IL-1$\beta$, IL-6, and TNF-$\alpha$. The reduced secretion of proinflammatory cytokines is related to the differences in the mRNA expression of IL-1$\beta$, IL-6, and TNF-$\alpha$. Moreover, licochalcone A inhibited the mRNA expression of IL-12p40, IL-18, and IL-23p19. To investigate its mechanism, we performed gel shift assay. Licochalcone A reduced nuclear NF-${\kappa}B$ binding activity in LPS-activated RAW264.7 cells. Taken together, these results suggest that licochalcone A has anti-inflammatory effects in LPS-activated macrophages and its mechanism could be through the down-regulation of binding to the ${\kappa}B$ site.