• Title/Summary/Keyword: BHOSB

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Effects of BHOSB on Various Immunological Factors Related to Pathogenesis of Atopic Dermatitis in DNCB Treated NC/Nga Mice (비허온습만(脾虛蘊濕万)이 아토피 피부염 유발 NC/Nga 생쥐의 혈액내 면역 관련 인자에 미치는 영향)

  • Park, Sung-Hee;Jin, Mi-Rim;Koo, Young-Sun;Kim, Dong-Hee
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.21 no.4
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    • pp.849-855
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    • 2007
  • Atopic dermatitis is an allergic inflammatory skin disease caused by aberrant and overreactive immune responses including overactivation of $T_H2$ immune responses, high levels of IgE as well as proinflammatory cytokines and chemokines. We examined whether BHOSB, a traditional herbal medicine, has modulatory effects on various immunological factors related to pathogenesis of atopic dermatitis in ONCB treated NC/Nga mice. Oral administration of BHOSB at the concentration of 10.8 mg/mouse/day significantly inhibited the production of IgE compared with control, and the levels of IgG2a and IgG2b, but not IgG1, were also significantly reduced. Production of IL-6 and TNF-a was greatly decreased. The results from flowcytometry of peripheral blood mononuclear cells indicated that the percentages of C03+C069+ cells and C04+ were significantly decreased by BHOSB. Theses results suggested that BHOSB has suppressive effects on aberrant and overreactive immunological activities in ONCB-induced dermatitis mice of NC/Nga.

Suppression of DNCB-induced Dermatitis in NC/Nga Murine Model by Biheoonsupbang (비허온습방(脾虛蘊濕方)이 NC/Nga 아토피피부염 생쥐 모델의 피부 및 면역학적 변화에 미치는 영향)

  • Kim, Jung-Hwan;Choi, Jeong-June;Koo, Young-Sun;Roh, Seong-Soo;Kim, Dong-Hee
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.21 no.3
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    • pp.714-720
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    • 2007
  • Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by inflammatory cell infiltration in the skin. This study was performed to assess the therapeutic effects of BHOSB on the DNCB-induced dermatitis in NC/Nga mice, characterized by the onset of AD along with an increase the number of inflammatory cells and dysregulation of inflammatory mediators including cytokines and chemokines. BHOSB administration significantly reduced clinical dermatitis severity including pruritus, edema, eczematous and erythema. Histological findings indicated that the thickening of epidermis/dermis and dermal infiltration of inflammatory cells including mast cells were dramatically reduced. The suppression of dermatitis by BHOSB was accompanied by a decrease in the number of CD11b$^+$/Gr-1$^+$ immune cells in skin but not CD3$^+$/CCR3$^+$ cells. However, the number of CD3$^+$ cells was increased in BHOSB administrated NC/Nga mice. Oral administration of BHOSB significantly reduced the level of IL-6, TNF-a and eotaxin 2 mRNA in skin. These data suggest that BHOSB may be effective therapeutic agents for the treatment of AD.