• Title/Summary/Keyword: Gagam-Danguieumja

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Effect of Gagam-Danguieumja through Regulation of MAPK on LPS-Induced Inflammation in RAW 264.7 Cells (LPS로 유도된 RAW 264.7 cell의 염증반응에서 MAPK 조절에 의한 가감당귀음자(加減當歸飮子)의 항염증 효과)

  • Kim, Tae-Yeon
    • The Journal of Internal Korean Medicine
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    • v.34 no.4
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    • pp.339-348
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    • 2013
  • Objectives : Danguieumja is a traditional medicinal prescription to treat skin disease. It was commonly used for the treatment of itching, chronic urticaria and atopic dermatitis in Korea by the addition or omission of several herbs. This study investigated the anti-inflammatory potential of Gagam-Danguieumja (GDE) water extract. Methods : We examined the effects of GDE on the lipopolysaccharide (LPS)-induced production of nitric oxide (NO) in a murine macrophage cell line, RAW 264.7 cells. Results : GDE inhibited production of NO in a dose dependent manner and also decreased the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2). As a possible molecular mechanism of anti-inflammatory effect increased phosphorylation of mitogen-activating protein kinases (MAPK) by LPS were blocked by GDE treatment. Conclusions : These results suggest that GDE has an anti-inflammatory therapeutic potential through the inhibition of MAPK phosphorylation, thereby decreasing the expression of pro-inflammatory genes.

Antioxidant and Protective Effects of Gagam-Danguieumja on Ultraviolet B-induced Damage in Human Keratinocytes (가감당귀음자의 항산화 효과와 자외선으로 유도된 각질형성세포 손상에 대한 보호효과)

  • Kim, Tae Yeon;Bak, Jong Phil
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.29 no.6
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    • pp.475-484
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    • 2015
  • In this paper, we studied the anti-oxidative capacities and protective effects of water extract of Gagam-Danguieumja(GDE) against Ultraviolet B(UVB)-induced oxidative damage in human keratinocytes(HaCaT). To evaluate the anti-oxidative activities of GDE, we measured scavenging activities on DPPH radical, hydroxyl radical, hydrogen peroxide, superoxide anion, lipid peroxidation and reducing power of GDE. To detect the protective effects of GDE against UVB, we irradiated with 40 mJ/㎠`s UVB to HaCaT cells then we measured reactive oxygen species(ROS) generation, apoptotic bodies and cell viability using DCFH-DA assay, Hoechst 33342 staining and MTT assay. GDE showed the anti-oxidative activities by scavenging DPPH radical, hydroxyl radical, hydrogen peroxide, superoxide anion, lipid peroxidation. Also GDE showed high reducing values. GDE reduced oxidative stress conditions by inhibition of ROS expression. Also the cell apoptosis by UVB-induced oxidative conditions was decreased by GDE treatment. These results could suggest that GDE had anti-oxidative activities and exhibited protective effects against UVB on HaCaT cells. GDE would be useful for the development of cosmetics treating UVB-induced skin aging.

Regulatory Effect of Atopic Allergic Reaction by Modified Gagam-danguieumja

  • Na, Ho-Jeong;Kwon, Dong-Yeul;Kim, Hyung-Min;Park, Eun-Jeong;Lee, Eun-Hee;Hong, Seung-Heon
    • Biomolecules & Therapeutics
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    • v.12 no.4
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    • pp.235-241
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    • 2004
  • Gagam-danguiemja (GDGJ), a traditional Korean prescription, has been used as therapeutics for atopic allergic diseases such as atopic dermatitis. To evaluate the atopic allergic effect of modified GDGJ, we investigated a possible effect of GDGJ on mast cell-mediated allergic reaction, cytokinases secretion and mRNA expression in vivo and in vitro. Mast cells are a potent source of mediators that regulate the inflammatory response in allergic reaction. In mice orally administered by GDGJ (0.01, 0.1 and 1.0 g/kg) for 1 h, compound 48/80-induced ear oedema was significantly reduced. TNF-${\alpha}$, IL-8, and IL-6 secretion were inhibited by GDGJ in the human mast cell line (HNC-1). But TNF-${\alpha}$, IL-8, and IL-6 mRNA expression were not inhibited by GDGJ at the dose of 0.01 mg/ml. These findings may help in understanding the mechanism of action of this herbal medication, leading to the control of mast cells in atopic allergic reaction like AD.