• Title/Summary/Keyword: Rehmannia glutinosa pharmacopuncture solution(RGPS)

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Inhibitory Effect of Rehmannia Glutinosa Pharmacopuncture Solution on β-hexosaminidase Release and Cytokine Production via FcεRI signaling in RBL-2H3 Cells (RBL-2H3세포에서 생지황약침액의 FcεRI 신호전달을 통한 β-hexosaminidase분비와 Cytokine생성 억제 효과)

  • Kang, Kyung-Hwa;Kim, Cheol-Hong
    • Journal of Pharmacopuncture
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    • v.14 no.2
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    • pp.15-24
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    • 2011
  • Background: Type I allergy is involved in allergic asthma, allergic rhinitis, and atopic dermatitis which are accompanied by an acute and chronic allergic inflammatory responses. Rehmannia glutinosa is a traditional medicine in the East Asian region. This study examined whether a Rehmannia Glutinosa pharmacopuncture solution (RGPS) had anti-allergic or anti-inflammatory effects in antigen-stimulated-RBL-2H3 cells. Methods: We determined the effect of RGPS on cell viability using the 3-[4,5-dimethylthiazolyl]-2,5-diphenyltetrazolium bromide (MTT) assay. We also examined the effect of RGPS on the release of ${\beta}$-hexosaminidase and the secretion of IL-4 and TNF-${\alpha}$ using ELISA. In addition, we evaluated the effect of RGPS on the mRNA expression of various cytokines; IL-2, IL-3, IL-4, IL-5, IL-13 and TNF-${\alpha}$ using RT-PCR. Furthermore, we assessed the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-${\kappa}$B using Western blotting after RGPS treatment. Results: We found that RGPS ($10^{-4}$ to $10^{-1}$ dilution) did not cause any cytotoxicity. We observed significant inhibition of ${\beta}$-hexosaminidase release and suppression of the protein secretion of IL-4 and TNF-${\alpha}$ and mRNA expression of multiple cytokines in antigen-stimulated-RBL-2H3 cells after RGPS treatment. Additionally, RGPS suppressed not only the phosphorylation of MAPKs, but also the transcriptional activation of NF-${\kappa}$B in antigen-stimulated-RBL-2H3 cells. Conclusions: These results suggest that RGPS inhibits degranulation and expression of cytokines including IL-4 and TNF-${\alpha}$ via down-regulation of MAPKs and NF-${\kappa}$B activation in antigen-stimulated-RBL-2H3 cells. In conclusion, RGPS may have beneficial effects in the exerting anti-allergic or anti-inflammatory activities.

Rehmannia Glutinosa Pharmacopuncture Solution Regulates Functional Activation, FcεRI Expression, and Signaling Events in Mast Cells

  • Kang, Kyung-Hwa;Lee, Kyung-Hee;Yoon, Hyun-Min;Jang, Kyung-Jeon;Song, Chun-Ho;Kim, Cheol-Hong
    • Journal of Pharmacopuncture
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    • v.15 no.4
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    • pp.32-41
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    • 2012
  • Objectives: Rehmannia glutinosa pharmacopuncture solution (RGPS) was investigated to determine both its anti-allergic inflammatory effects on mast cells and its detailed mechanism of actions. Methods: We investigated whether RGPS suppress cytokines, enzymes, $Fc{\varepsilon}RI$ expression and $Fc{\varepsilon}RI$-mediated signaling in RBL-2H3 cells stimulated with anti-DNP IgE/DNP-HSA. The suppressive effects of RGPS on the levels of cytokines such as IL-$1{\beta}$, IL-6 and GM-CSF were measured using emzyme-linked immunospecific assay (ELISA). The mRNA expression levels of cytokines, enzymes (HDC2, COX-1, COX-2 and 5LO) and $Fc{\varepsilon}RI$ ${\alpha}{\beta}{\gamma}$ subunits were measured using reverse transcription polymerase chain reaction (RT-PCR) method. The activation of $Fc{\varepsilon}RI$-mediated signaling was examined using Western blot analyses. Results: RGPS suppressed production of proinflammatory cytokines (IL-$1{\beta}$, IL-6, and GM-CSF) in stimulated RBL-2H3 cells significantly (p < 0.05). RGPS also suppressed mRNA expression of inflammatory enzymes (HDC2, COX-1, COX-2, 5LO). In addition, mRNA expression levels of $Fc{\varepsilon}RI{\alpha}$, $Fc{\varepsilon}RI{\beta}$and $Fc{\varepsilon}RI{\gamma}$ were lowered by treatment with RGPS. Finally, RGPS prevented phosphrylation of Lyn, Syk, LAT, Gab2, PLC ${\gamma}1/2$, PI3K, Akt, cPLA2 and $I{\kappa}B{\alpha}$. Conclusions: RGPS effectively suppresses mast cell activations such as degranulation and inflammatory response via down-regulation of the $Fc{\varepsilon}RI$-mediated signaling pathways in IgE/Ag-stimulated mast cells.