• Title/Summary/Keyword: Inflammatory gene expression

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North American ginseng influences adipocyte-macrophage crosstalk regulation of inflammatory gene expression

  • Garbett, Jaime;Wilson, Sarah A.F.;Ralston, Jessica C.;Boer, Anna A. De;Lui, Ed M.K.;Wright, David C.;Mutch, David M.
    • Journal of Ginseng Research
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    • v.40 no.2
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    • pp.141-150
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    • 2016
  • Background: Adipocyte-macrophage communication plays a critical role regulating white adipose tissue (WAT) inflammatory gene expression. Because WAT inflammation contributes to the development of metabolic diseases, there is significant interest in understanding how exogenous compounds regulate the adipocyte-macrophage crosstalk. An aqueous (AQ) extract of North American (NA) ginseng (Panax quinquefolius) was previously shown to have strong inflammo-regulatory properties in adipocytes. This study examined whether different ginseng extracts influence adipocyte-macrophage crosstalk, as well as WAT inflammatory gene expression. Methods: The effects of AQ and ethanol (EtOH) ginseng extracts ($5{\mu}g/mL$) on adipocyte and macrophage inflammatory gene expression were studied in 3T3-L1 and RAW264.7 cells, respectively, using real-time reverse transcription polymerase chain reaction. Adipose tissue organ culture was also used to examine the effects of ginseng extracts on epididymal WAT (EWAT) and inguinal subcutaneous WAT (SWAT) inflammatory gene expression. Results: The AQ extract caused significant increases in the expression of common inflammatory genes (e.g., Mcp1, Ccl5, Tnf-${\alpha}$, Nos2) in both cell types. Culturing adipocytes in media from macrophages treated with the AQ extract, and vice versa, also induced inflammatory gene expression. Adipocyte Ppar-${\gamma}$ expression was reduced with the AQ extract. The AQ extract strongly induced inflammatory gene expression in EWAT, but not in SWAT. The EtOH extract had no effect on inflammatory gene expression in either both cell types or WAT. Conclusion: These findings provide important new insights into the inflammo-regulatory role of NA ginseng in WAT.

Anti-inflammatory Flavonoids: Modulators of Proinflammatory Gene Expression

  • Kim, Hyun-Pyo;Son, Kun-Ho;Chang, Hyeun-Wook;Kang, Sam-Sik
    • Natural Product Sciences
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    • v.10 no.1
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    • pp.1-10
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    • 2004
  • Plant flavonoids possess anti-inflammatory activity in vitro and in vivo. Although the action mechanisms are not fully understood, recent studies have clearly shown that certain flavonoids, especially flavone derivatives, express their anti-inflammatory activity at least in part by modulation of proinflammatory gene expression such as cyclooxygenase-2, inducible nitric oxide synthase and various cytokines. This review summarizes the recent findings of flavonoids modulating expression of proinflammatory molecules.

Effects of Moschus moschiferus Extracts on the Inflammatory Cytokines Gene Expression of Murine Macrophages (사향추출물이 생쥐 대식세포의 염증 유발 싸이토카인 유전자 발현에 미치는 영향)

  • Lim, Seok-lin
    • Journal of Haehwa Medicine
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    • v.9 no.2
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    • pp.315-324
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    • 2001
  • To investigate the capacity of anti-inflammatory cytokines and biological response modifiers (BRMs) to induce IL-$1{\beta}$, IL-6, TNF-${\alpha}$ gene overexpression from mouse macrophages, we isolated the resident peritoneal macrophages from BALB/c mouse (8 week old) and incubated for 6 h with lipopolysaccaride (LPS) and Moschus moschiferus (MOMS) extracts. Analysis of inflammatory cytokines gene expression was carried out by RT-PCR amplification. Amplified PCR products were electrophoresed on 1.2% agarose gel, and the analysis (Ht) was used to 1D-density program. 1. LPS and MOMS extract treatments resulted in a significant decrease in IL-$1{\beta}$, IL-6, TNF-${\alpha}$ mRNA expression level compared with the LPS treatment. 2. Among four sample of MOMS, Inhibitory effects of MOMS-A and MOMS-D for inflammatory cytokines gene expression were to be fine compared with the MOMS-Band MOMS-C. According to the above data, Because the anti- tumoral and anti-inflammatory response activities of macrophage are known to be dependent on the production of inflammatory cytokines (IL-$1{\beta}$, IL-6, TNF-${\alpha}$) by macrophages, we suggest that evaluations of BRM for the reduction of inflammatory cytokines production by macrophages are important for clinical application.

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Flavonoid and Skin Inflammation

  • Kim, Hyun-Pyo
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 2007.11a
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    • pp.67-73
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    • 2007
  • There have been various inflammatory skin disorders in humans including atopic dermatitis, eczema and psoriasis. Although some drugs have been used for these disorders, there is an urgent need for safer and more effective topical anti-inflammatory agents. Plant flavonoids possess anti-inflammatory activity and some of them have multiple pharmacological mechanisms, inhibition of eicosanoid metabolizing enzymes, histamine release and/or down-regulation of pro inflammatory gene expression. These properties of flavonoids may be suitable for treating chronic skin inflammatory disorders. Especially, wogonin, some prenylated flavonoids and biflavonoids have a strong potential as new anti-inflammatory agents by topical application.

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Anti-inflammatory effect of sulforaphane on LPS-stimulated RAW 264.7 cells and ob/ob mice

  • Ranaweera, Sachithra S.;Dissanayake, Chanuri Y.;Natraj, Premkumar;Lee, Young Jae;Han, Chang-Hoon
    • Journal of Veterinary Science
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    • v.21 no.6
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    • pp.91.1-91.15
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    • 2020
  • Background: Sulforaphane (SFN) is an isothiocyanate compound present in cruciferous vegetables. Although the anti-inflammatory effects of SFN have been reported, the precise mechanism related to the inflammatory genes is poorly understood. Objectives: This study examined the relationship between the anti-inflammatory effects of SFN and the differential gene expression pattern in SFN treated ob/ob mice. Methods: Nitric oxide (NO) level was measured using a Griess assay. The inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression levels were analyzed by Western blot analysis. Pro-inflammatory cytokines (tumor necrosis factor [TNF]-α, interleukin [IL]-1β, and IL-6) were measured by enzyme-linked immunosorbent assay (ELISA). RNA sequencing analysis was performed to evaluate the differential gene expression in the liver of ob/ob mice. Results: The SFN treatment significantly attenuated the iNOS and COX-2 expression levels and inhibited NO, TNF-α, IL-1β, and IL-6 production in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. RNA sequencing analysis showed that the expression levels of 28 genes related to inflammation were up-regulated (> 2-fold), and six genes were down-regulated (< 0.6-fold) in the control ob/ob mice compared to normal mice. In contrast, the gene expression levels were restored to the normal level by SFN. The protein-protein interaction (PPI) network showed that chemokine ligand (Cxcl14, Ccl1, Ccl3, Ccl4, Ccl17) and chemokine receptor (Ccr3, Cxcr1, Ccr10) were located in close proximity and formed a "functional cluster" in the middle of the network. Conclusions: The overall results suggest that SFN has a potent anti-inflammatory effect by normalizing the expression levels of the genes related to inflammation that were perturbed in ob/ob mice.

Interleukin-32 in Inflammatory Autoimmune Diseases

  • Kim, Soohyun
    • IMMUNE NETWORK
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    • v.14 no.3
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    • pp.123-127
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    • 2014
  • Interleukin-32 (IL-32) is a cytokine inducing crucial inflammatory cytokines such as tumor necrosis factor-${\alpha}(TNF{\alpha})$ and IL-6 and its expression is elevated in various inflammatory autoimmune diseases, certain cancers, as well as viral infections. IL-32 gene was first cloned from activated T cells, however IL-32 expression was also found in other immune cells and non-immune cells. IL-32 gene was identified in most mammals except rodents. It is transcribed as multiple-spliced variants in the absence of a specific activity of each isoform. IL-32 has been studied mostly in clinical fields such as infection, autoimmune, cancer, vascular disease, and pulmonary diseases. It is difficult to investigate the precise role of IL-32 in vivo due to the absence of IL-32 gene in mouse. The lack of mouse IL-32 gene restricts in vivo studies and restrains further development of IL-32 research in clinical applications although IL-32 new cytokine getting a spotlight as an immune regulatory molecule processing important roles in autoimmune, infection, and cancer. In this review, we discuss the regulation and function of IL-32 in inflammatory bowel diseases and rheumatoid arthritis.

The Effect of Galkunhwanglyeonhwanggum-tang (GGT) and Sopunghwalhyeol-tang (SPT) on Gene Expression Levels of MCP-1, ICAM-1, VCAM-1, and eNOS in HUVECs (갈근황연황금탕(葛根黃蓮黃芩湯)과 소풍활혈탕(疎風活血湯)이 HUVEC 내에 MCP-1, ICAM-1, VCAM-1 and eNOS의 유전자 발현량에 대해 미치는 영향)

  • Jeong, Hyun-jin;Jeon, Sang-yoon;Jang, Hye-yeon;Kim, Min-wook
    • The Journal of Internal Korean Medicine
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    • v.41 no.4
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    • pp.668-675
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    • 2020
  • Objectives: The aim of this study was to compare the effects of Galkunhwanglyeonhwanggum-tang (GGT), and Sopunghwalhyeol-tang (SPT) on gene expression of MCP-1, ICAM-1, VCAM-1, and eNOS in human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were treated with GGT and SPT at concentrations of 50, 100, and 200 ㎍/mL. Gene expression of MCP-1, ICAM-1, VCAM-1, and eNOS in HUVECs was analyzed by the polymerase chain reaction (PCR), and electrophoresis was performed to verify the gene expression level. Results: 1. MCP-1 gene expression was more strongly decreased by SPT than by GGT. 2. ICAM-1 and VCAM-1 gene expressions were more strongly decreased by SPT than by GGT 3. GGT significantly increased eNOS gene expression, but SPT did not. Conclusions: These findings suggest that GGT and SPT regulate gene expression related to anti-inflammatory effects in HUVECs. Clinical application of these Korean medicines to diseases related to dyslipidemia, such as cardiovascular disease, will require additional in vivo experiments to verify the anti-inflammatory effects of GGT and SPT.

Inhibition of Contact Dermatitis in Animal Models and Suppression of Proinflammatory Gene Expression by Topically Applied Flavonoid, Wogonin

  • Lim, Hyun;Park, Haeil;Kim, Hyun-Pyo
    • Archives of Pharmacal Research
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    • v.27 no.4
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    • pp.442-448
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    • 2004
  • Wogonin (5,7-dihydroxy-8-methoxyflavone) is a down-regulator of cyclooxygenase-2 and inducible nitric oxide synthase expression, contributing to anti-inflammatory activity in vivo. For further characterization of modulatory activity on ploinflammatory gene expression in vivo, the effect of wogonin was examined in this experiment using animal models of skin inflammation. By topical application, wogonin inhibited an edematic response as well as ploinflammatory gene expression against contact dermatitis In mice. Wogonin inhibited ear edema ($19.4-22.6\%$) at doses of $50-200\;{\mu}g$/ear and down-regulated interleukin-$1{\beta}$ induction ($23.1\%$) at $200{\mu}g$/ear in phenol-induced simple irritation. Wogonin ($2{\times}50-2{\times}200{\mu}g$/ear) also inhibited edematic response ($51.2-43.9\%$) and down-regulated ploinflammatory gene expression of cyclooxygenase-2, interleukin-$1{\beta}$, interferon-$\gamma$, intercellular adhesion molecule-1 and inducible nitric oxide synthase with some different sensitivity against picryl chloride-induced delayed hypersensitivity reaction. All these results clearly demonstrate that wogonin is a down-regulator of ploinflammatory gene expression in animal models of skin inflammation. Therefore, wogonin may have potential for a new anti-inflammatory agent against skin inflammation.

Recent Advances in Anti-inflammatory Flavonoid Research since 2004

  • Kim Hyun-Pyo
    • Biomolecules & Therapeutics
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    • v.14 no.1
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    • pp.11-18
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    • 2006
  • Certain flavonoids possess anti-inflammatory activity. Besides their antioxidative property, the cellular action mechanisms of flavonoids include an inhibition of arachidonate metabolizing enzymes such as cyclooxygenases and lipoxygenases, and a down-regulation of proinflammatory gene expression such as cyclooxygenase-2, inducible nitric oxide synthase and tumor necrosis factor-$\alpha$. In this review, the recent findings of anti-inflammatory flavonoid research since 2004 were summarized. And the cellular mechanisms on signal transduction pathways were also discussed.

Antioxidant and Anti-inflammatory Effects of Yam (Dioscorea batatas Decne.) on Azoxymethane-induced Colonic Aberrant Crypt Foci in F344 Rats

  • Son, In Suk;Lee, Jeong Soon;Lee, Ju Yeon;Kwon, Chong Suk
    • Preventive Nutrition and Food Science
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    • v.19 no.2
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    • pp.82-88
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    • 2014
  • Yam (Dioscorea batatas Decne.) has long been used as a health food and oriental folk medicine because of its nutritional fortification, tonic, anti-diarrheal, anti-inflammatory, antitussive, and expectorant effects. Reactive oxygen species (ROS), which are known to be implicated in a range of diseases, may be important progenitors of carcinogenesis. The aim of this study was to investigate the modulatory effect of yam on antioxidant status and inflammatory conditions during azoxymethane (AOM)-induced colon carcinogenesis in male F344 rats. We measured the formation of aberrant crypt foci (ACF), hemolysate antioxidant enzyme activities, colonic mucosal antioxidant enzyme gene expression, and colonic mucosal inflammatory mediator gene expression. The feeding of yam prior to carcinogenesis significantly inhibited AOM-induced colonic ACF formation. In yam-administered rats, erythrocyte levels of glutathione, glutathione peroxidase (GPx), and catalase were increased and colonic mucosal gene expression of Cu/Zn-superoxide dismutase (SOD), Mn-SOD, and GPx were up-regulated compared to the AOM group. Colonic mucosal gene expression of inflammatory mediators (i.e., nuclear factor kappaB, inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor alpha, and interleukin-1beta) was suppressed by the yam-supplemented diet. These results suggest that yam could be very useful for the prevention of colon cancer, as they enhance the antioxidant defense system and modulate inflammatory mediators.