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Topical application of herbal mixture extract inhibits ovalbumin- or 2,4-dinitrochlorobenzene-induced atopic dermatitis.

Kim SR, Choi HS, Seo HS, Choi YK, Shin YC, Ko SG - Evid Based Complement Alternat Med (2012)

Bottom Line: Atopic dermatitis (AD) is an inflammatory skin disease associated with enhanced T-helper2 (Th2) lymphocyte response to allergens that results in elevated serum eosinophil and Immunoglobulin E (IgE) levels and leukocyte infiltration in atopic skin sites.Histological analyses demonstrated decreased mast cell count as well as dermal infiltration by inflammatory cells.Taken together, our results showed that topical application of KM110329 extracts exerts beneficial effects in AD symptoms, suggesting that KM110329 might be a useful candidate for the treatment of AD.

View Article: PubMed Central - PubMed

Affiliation: Department of Preventive Medicine, College of Oriental Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.

ABSTRACT
KM110329 is four traditional herbal medicine mixtures with anti-inflammatory properties. Atopic dermatitis (AD) is an inflammatory skin disease associated with enhanced T-helper2 (Th2) lymphocyte response to allergens that results in elevated serum eosinophil and Immunoglobulin E (IgE) levels and leukocyte infiltration in atopic skin sites. In this study, we investigated the effect of topical application of KM110329 ethanol extract on the ovalbumin (OVA) or 2,4-dinitrochlorobenzene- (DNCB-) induced AD mouse models. For that purpose, we observed the effects of KM110329 on blood eosinophils, skin mast cells, production of serum IgE, and expression of cytokine mRNA in the atopic dermatitis skin lesions of OVA allergen- or DNCB-treated BALB/c mice. KM110329 significantly reduced blood eosinophils cell numbers in OVA or DNCB-treated BALB/c mice. Histological analyses demonstrated decreased mast cell count as well as dermal infiltration by inflammatory cells. In the skin lesions, mRNA expression of interleukine (IL)-4, IL-13, and IL-17 was inhibited by KM110329. KM110329 also suppressed the production of serum IgE level in both the OVA- and DNCB-induced atopic dermatitis model. Taken together, our results showed that topical application of KM110329 extracts exerts beneficial effects in AD symptoms, suggesting that KM110329 might be a useful candidate for the treatment of AD.

No MeSH data available.


Related in: MedlinePlus

Protocol for induction of atopic dermatitis. Shaved dorsal regions of the mice were sensitized epicutaneously with OVA (a) or DNCB (b) solution. (a) Female BALB/c mice were intraperitioneally sensitized with OVA once a week for three weeks. After three weeks, the back of the mice was shaved with an electric razor and dermally challenged with 1 × 1 cm sterile patches containing OVA (100 μg) for 3 weeks. KM110329 was applied to the skin during the second and third skin sensitization week together with OVA. (b) Male BALB/c mice were epicutaneously sensitized with 200 μL of a 1% DNCB solution on day 1. Two weeks later, dermatitis was induced with 200 μL of 0.2% DNCB solution at the intervals shown in figure. KM110329 was applied to the skin from the 3th week during sensitization together with DNCB.
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fig1: Protocol for induction of atopic dermatitis. Shaved dorsal regions of the mice were sensitized epicutaneously with OVA (a) or DNCB (b) solution. (a) Female BALB/c mice were intraperitioneally sensitized with OVA once a week for three weeks. After three weeks, the back of the mice was shaved with an electric razor and dermally challenged with 1 × 1 cm sterile patches containing OVA (100 μg) for 3 weeks. KM110329 was applied to the skin during the second and third skin sensitization week together with OVA. (b) Male BALB/c mice were epicutaneously sensitized with 200 μL of a 1% DNCB solution on day 1. Two weeks later, dermatitis was induced with 200 μL of 0.2% DNCB solution at the intervals shown in figure. KM110329 was applied to the skin from the 3th week during sensitization together with DNCB.

Mentions: The schematic experimental procedure is described in Figure 1. For establishment of OVA-induced AD model, female 7 weeks old BALB/c mice were intraperitoneally sensitized with 20 μg of OVA once a week for three weeks. After three weeks, the back of the mice was shaved with an electric razor and dermally challenged with 1 × 1 cm sterile patches containing OVA (100 μg) for 2 weeks. KM110329 was applied to the skin during the second and third skin sensitization week together with OVA. Patches were changed three times per week during sensitization (Figure 1(a)). For formation of DNCB-induced AD model, male 7 weeks old BALB/c mice were divided into three groups, each comprising of four mice. After shaving, mice back skin was painted dermally with 200 μL of a 1% DNCB using 1 × 1 cm patches. Two weeks after sensitization, the back skin was challenged with 200 μL of a 0.2% DNCB solution twice a week. This procedure was repeated for 4 weeks. KM110329 was applied to the skin from the 3th week during sensitization together with DNBC (Figure 1(b)). Mice were killed by CO2-inhalation, and samples were collected.


Topical application of herbal mixture extract inhibits ovalbumin- or 2,4-dinitrochlorobenzene-induced atopic dermatitis.

Kim SR, Choi HS, Seo HS, Choi YK, Shin YC, Ko SG - Evid Based Complement Alternat Med (2012)

Protocol for induction of atopic dermatitis. Shaved dorsal regions of the mice were sensitized epicutaneously with OVA (a) or DNCB (b) solution. (a) Female BALB/c mice were intraperitioneally sensitized with OVA once a week for three weeks. After three weeks, the back of the mice was shaved with an electric razor and dermally challenged with 1 × 1 cm sterile patches containing OVA (100 μg) for 3 weeks. KM110329 was applied to the skin during the second and third skin sensitization week together with OVA. (b) Male BALB/c mice were epicutaneously sensitized with 200 μL of a 1% DNCB solution on day 1. Two weeks later, dermatitis was induced with 200 μL of 0.2% DNCB solution at the intervals shown in figure. KM110329 was applied to the skin from the 3th week during sensitization together with DNCB.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3526256&req=5

fig1: Protocol for induction of atopic dermatitis. Shaved dorsal regions of the mice were sensitized epicutaneously with OVA (a) or DNCB (b) solution. (a) Female BALB/c mice were intraperitioneally sensitized with OVA once a week for three weeks. After three weeks, the back of the mice was shaved with an electric razor and dermally challenged with 1 × 1 cm sterile patches containing OVA (100 μg) for 3 weeks. KM110329 was applied to the skin during the second and third skin sensitization week together with OVA. (b) Male BALB/c mice were epicutaneously sensitized with 200 μL of a 1% DNCB solution on day 1. Two weeks later, dermatitis was induced with 200 μL of 0.2% DNCB solution at the intervals shown in figure. KM110329 was applied to the skin from the 3th week during sensitization together with DNCB.
Mentions: The schematic experimental procedure is described in Figure 1. For establishment of OVA-induced AD model, female 7 weeks old BALB/c mice were intraperitoneally sensitized with 20 μg of OVA once a week for three weeks. After three weeks, the back of the mice was shaved with an electric razor and dermally challenged with 1 × 1 cm sterile patches containing OVA (100 μg) for 2 weeks. KM110329 was applied to the skin during the second and third skin sensitization week together with OVA. Patches were changed three times per week during sensitization (Figure 1(a)). For formation of DNCB-induced AD model, male 7 weeks old BALB/c mice were divided into three groups, each comprising of four mice. After shaving, mice back skin was painted dermally with 200 μL of a 1% DNCB using 1 × 1 cm patches. Two weeks after sensitization, the back skin was challenged with 200 μL of a 0.2% DNCB solution twice a week. This procedure was repeated for 4 weeks. KM110329 was applied to the skin from the 3th week during sensitization together with DNBC (Figure 1(b)). Mice were killed by CO2-inhalation, and samples were collected.

Bottom Line: Atopic dermatitis (AD) is an inflammatory skin disease associated with enhanced T-helper2 (Th2) lymphocyte response to allergens that results in elevated serum eosinophil and Immunoglobulin E (IgE) levels and leukocyte infiltration in atopic skin sites.Histological analyses demonstrated decreased mast cell count as well as dermal infiltration by inflammatory cells.Taken together, our results showed that topical application of KM110329 extracts exerts beneficial effects in AD symptoms, suggesting that KM110329 might be a useful candidate for the treatment of AD.

View Article: PubMed Central - PubMed

Affiliation: Department of Preventive Medicine, College of Oriental Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.

ABSTRACT
KM110329 is four traditional herbal medicine mixtures with anti-inflammatory properties. Atopic dermatitis (AD) is an inflammatory skin disease associated with enhanced T-helper2 (Th2) lymphocyte response to allergens that results in elevated serum eosinophil and Immunoglobulin E (IgE) levels and leukocyte infiltration in atopic skin sites. In this study, we investigated the effect of topical application of KM110329 ethanol extract on the ovalbumin (OVA) or 2,4-dinitrochlorobenzene- (DNCB-) induced AD mouse models. For that purpose, we observed the effects of KM110329 on blood eosinophils, skin mast cells, production of serum IgE, and expression of cytokine mRNA in the atopic dermatitis skin lesions of OVA allergen- or DNCB-treated BALB/c mice. KM110329 significantly reduced blood eosinophils cell numbers in OVA or DNCB-treated BALB/c mice. Histological analyses demonstrated decreased mast cell count as well as dermal infiltration by inflammatory cells. In the skin lesions, mRNA expression of interleukine (IL)-4, IL-13, and IL-17 was inhibited by KM110329. KM110329 also suppressed the production of serum IgE level in both the OVA- and DNCB-induced atopic dermatitis model. Taken together, our results showed that topical application of KM110329 extracts exerts beneficial effects in AD symptoms, suggesting that KM110329 might be a useful candidate for the treatment of AD.

No MeSH data available.


Related in: MedlinePlus