• 한국약용작물학회:학술대회논문집
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• 한국약용작물학회 2011년도 추계학술발표회
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• pp.240-241
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• 2011

• Toxicological Research
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• 제32권2호
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• pp.149-158
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• 2016

Atopic dermatitis (AD) is a chronic inflammatory skin disease with a complex etiology that encompasses immunologic responses. AD is frequently associated with elevated immunoglobulin (Ig) E levels, and common environmental factors contribute to its pathogenesis. Several recent studies have documented the role of specific lactic acid bacteria in the treatment and prevention of AD in humans and mice. In this study, the efficacy of Duolac ATP, a probiotic preparation, was determined in a mouse model with AD-like skin lesions. Alterations in the cytokine levels and histological staining suggested the alleviation of AD. The in vivo test showed that T helper (Th)2 cytokines, IgE, interleukin (IL)-4, and IL-5, were significantly downregulated, whereas Th1 cytokines, IL-12p40 and interferon (IFN)-${\gamma}$, were upregulated in all groups of mice treated with Duolac ATP compared to that observed in the group of mice treated with 1-chloro-2,4-dinitrobenzene (DNCB) alone. Moreover, the scratch score decreased in all mice treated with Duolac ATP. Staining of the dorsal area of the mice in each group with hematoxylin and eosin and toluidine blue further confirmed the alleviation of AD in mice orally treated with Duolac ATP. These results suggest that Duolac ATP inhibits the development of AD-like skin lesions in NC/Nga mice by suppressing the Th2 cell response and increasing the Th1 cell response. Thus, Duolac ATP is beneficial and effective for the treatment of AD-like skin lesions.

• 대한한방소아과학회지
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• 제33권2호
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• pp.22-31
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• 2019

Objective This study is to learn the effects of Hataedock method using Coptidis rhizoma and Glycyrrhiza uralensis mixed extract on inflammatory response in allergic rhinitis-induced obese NC/Nga mice. Materials and Methods The mice were fed with high fat-diet to be obese, and were divided into 3 groups as follows; allergic rhinitis-induced obese mice group with Hataedock method (CGT, n=10), no treatment group (Ctrl), allergic rhinitis elicited obese mice group (ARE). To induce allergic rhinitis, NC/Nga mice of 3 weeks age were sensitized on 7, 8 and 9 weeks by ovalbumin antigen in intraperitoneal space. After 7 days of final sensitization, allergic rhinitis was initially induced in mice through nasal cavities for 5 days. After 1-week, allergic rhinitis was induced again by the same method. Histological examination was used to identify distribution of IL-4, CD40, STAT6, $Fc{\varepsilon}RI$, substance P, MMP-9, NF-${\kappa}B$ p65, iNOS and COX-2. Results Hataedock method significantly reduced IL-4, STAT6 and CD40 response (p<0.05). In CGT, the inhibition of Th2 differentiation decreased inflammatory mediators such as $Fc{\varepsilon}RI$, substance P, MMP-9, NF-${\kappa}B$ p65, iNOS and COX-2 (all p<0.05). The immunological improvement led reduction of respiratory epithelial damage and mucin secretion in goblet cell. Conclusion The results of this study show that the Hataedock method suppresses the expression of allergic rhinitis by decreasing the inflammatory mediators through the regulation of Th2 differentiation even when the inflammation reaction is increased by obesity. Therefore, Hataedock may have potential preventive measure of allergic rhinitis accompanied by obese.

• 한국약용작물학회:학술대회논문집
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• 한국약용작물학회 2007년도 춘계학술발표회
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• pp.265-266
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• 2007

• 대한한방내과학회지
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• 제36권4호
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• pp.486-497
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• 2015

Objectives Hataedock is an orally administered herbal extract treatment for newborn babies that dispels toxic heat and meconium gathered by the fetus. The purpose of this study was to evaluate whether Hataedock alleviates inflammatory skin damage in AD (Atopic Dermatitis)-induced NC/Nga mice through regulating and maintaining the skin barrier and anti-inflammation effects.Methods We established an AD model in three-week-old NC/Nga mice through the repeated application of DNFB (dinitrochlorobenzene) on days 28, 35, and 42 after Hataedock treatment was orally administered. We identified changes in the skin barrier and anti-inflammation effects through the histological and immunohistochemical changes of TNF- α, NF-κB p65, iNOS, COX-2, and apoptotic bodies.Results Skin damage and angiogenesis were mitigated in the HT (Hataedock) group. Damage to the intercellular space of the stratum corneum as well as hyperplasia, edema, the infiltration of lymphocytes, and the increase of capillaries decreased in the HT group. Our results suggest that Hataedock treatment significantly down-regulated levels of TNF- α by 38% (p<0.001) and of NF-κB p65 by 70% (p<0.001). But Hataedock up-regulated apoptosis by 183% in dermatitis-induced skin.Conclusions These results suggest that Hataedock alleviates AD through diminishing the various inflammatory cytokines in skin lesions that are involved in the initial steps of AD development. It might have potential applications for the prevention and treatment of atopic dermatitis.

• 대한화장품학회지
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• 제43권4호
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• pp.281-287
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• 2017

피부에 가해지는 스트레스는 헤어조절 및 사이클에 직 간접적으로 중요한 영향을 미친다고 알려져 있다. 특히, 모근세포는 스트레스에 의한 부신피질관련호르몬과 세포손상 및 사멸과 밀접한 관련이 있다고 보고되고 있지만, 현재까지 실험적으로 입증된 사실은 매우 제한되어 있다. 보고에 의하면, 부신피질자극호르몬방출인자가 증가되면 모근세포의 마이토콘드리아 활성을 저해하여 초기단계의 세포사멸을 가져올 수 있다고 임상학적으로 보고된바가 있다. 특히 아토피 피부염으로 인한 스트레스는 부신피질자극호르몬방출인자와 부신피질관련 호르몬의 양을 증가시키며, 이는 모발의 outer epithelial sheath에 영향을 준다고 알려져 있으며, 이러한 스트레스의 변화는 마이토콘드리아 손상을 초래하여 초기단계세포손상을 준다고 한다. 따라서 본 연구는 아토피피부염스트레스가 피부의 모근세포에 주는 영향에 대하여 연구를 하였는데, 이에 대한 연구는 현재까지 전무한 실정이다. 우리는 NC/Nga 마우스에 2,4-dinitrochlorobenzene (DNCB)로 아토피피부염을 유발 후, 피부 스트레스 생성에 의한 초기단계 세포손상을 스트레스관련 인자, 부신피질자극호르몬방출인자 및 그 관련 인자, annexin V 및 마이토콘드리아 반응을 이용하여 연구하였다. 그 결과, 아토피피부염에 의한 스트레스는 체내의 부신피질 자극호르몬방출인자 및 관련인자의 활성을 증가시킬 뿐 아니라, 모근세포에 영향을 주어 초기단계세포사멸을 초래하는 것으로 나타났다. 이는 아토피피부염관련 헤어손상을 일으킨다는 중요한 연구결과를 보고하는 바이며, 부신피질자극호르몬 조절관련 의약품 및 화장품 등과 같은 보조적 요법이 필요함을 제안한다.

• 대한한방소아과학회지
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• 제23권3호
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• pp.9-36
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• 2009

Objectives The purpose of this study is to examine the effect of a concurrent administration of JUJSTK and AJ on atopic dermatitis in an in-vivo experiment. Thus, this study is expressed by using NC/Nga atopic dermatitis mice which have histological and clinical similarities to that of humans have been used. Methods Clinical skin score, hematology, serum total IgE and IgG1 of the mouse was evaluated, and cytokine levels, total number of the cells, immunohistochemical staining, histological features of axillary lymph node(ALN), peripheral blood mononuclear cells(PBMCs), and a dorsal skin tissue of the mouse were analyzed. Results Oral administration of JUJSTK and concurrent administration of JUJSTK and AJ lowered the clinical skin score, total cell number of WBC, eosinophils in blood, and serum total of IgE & IgG1, IFN-$\gamma$, IL-5, IL-13, IL-17. In addition, total cell number of ALN and dorsal skin tissue, absolute cell number of $CD3e^+$ T cell, $CD4^+$ Th cell, $CD8^+$ c/sT cell, $CD3^+CCR3^+$ cell, $CCR3^+$ cell, $CD3^+CD69^+$, $CD4^+CXCR5^+$ in ALN, PBMCs, absolute cell number of $CCR3^+$, $CD3^+/CD69^+$, $CD11b^+/Gr-1^+$, $CD11b^+/Gr-1^+$ in dorsal skin tissue, Eotaxin2 mRNA, CCR3 mRNA in dorsal skin tissue and gene expression of IL-5 mRNA, IL-13 mRNA in ALN were significantly decreased. Furthermore, thickness of epidermis infiltrated inflammatory immune cell & mast cell in dermis, histological infiltration of mast cell, the size of inflammatory lymphocytes cells & plasma cells in ALN and histological infiltration of $CD4^+$ & $CCR3^+$ in ALN and dorsal skin tissue were significantly decreased as well. Conclusions Concurrent administration of JUJSTK and AJ on atopic dermatitis in an in-vivoexperiment by using an NC/Nga atopic dermatitis mouse was very effective as an atopic dermatitis treatment.

• 동의생리병리학회지
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• 제33권2호
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• pp.102-108
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• 2019

This study aims to evaluate the anti-inflammatory effect of Coptidis Rhizoma (CR) extract for atopic dermatitis through maintaining skin barrier and regulating Th2 cell differentiation. We divided NC/Nga mice into 3 groups as follows; atopy-like dermatitis induced group with CR treatment (CT, n=10), no treatment group(Ctrl), atopy-like dermatitis elicited group(AE). Atopy-like dermatitis was induced to NC/Nga mice by sensitizing with dermatophagoides farinae(DfE) on 7, 8, 9, 11, 12, and 13th week. After inducing atopic dermatitis, CR extract was administered 20 mg/kg daily for the experimental duration to the CT group. We measured the integrity of lipid layers in the epidermis and Th2 differentiation through immunohistochemical staining against filaggrin, loricrin, IL-4, and IL-13. We also measured the distribution of subcutaneous collagen fibers by the Masson's trichrome staining. Administration of CR significantly inhibited the reduction of lipid layers in the skin that caused atopy. The expression of IL-4, IL-13, each of which is a cytokine secreted by T helper type 2 (Th2) cells, was markedly suppressed in the CT group as compared with AE group (p<0.05). CR treatment also decreased the expression of iNOS, $p-I{\kappa}B$. Atopic dermatitis induced dermatological damage to skin, such as hyperplasia of epithelium, and capillary proliferation was significantly reduced by CR administration. CR effectively inhibited the thinning of the skin barrier and inflammatory responses in atopic dermatitis-induced mice. In particular, it showed anti-inflammatory effects by reducing the expression of IL-4 and IL-13, Th2 cell cytokines, which play a crucial role in development of atopic dermatitis. Therefore, CR can be a good candidate to ameliorate and treat atopic dermatitis.

• Biomolecules & Therapeutics
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• 제25권6호
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• pp.634-640
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• 2017

Atopic dermatitis (AD) is a common inflammatory skin disorder mediated by inflammatory cells, such as macrophages and mast cells. Rifampicin is mainly used for the treatment of tuberculosis. Recently, it was reported that rifampicin has anti-inflammatory and immune-suppressive activities. In this study, we investigated the effect of rifampicin on atopic dermatitis in vivo and in vitro. AD was induced by treatment with 2, 4-dinitrochlorobenzene (DNCB) in NC/Nga mice. A subset of mice was then treated with rifampicin by oral administration. The severity score and scratching behavior were alleviated in the rifampicin-treated group. Serum immunoglobulin E (IgE) and interleukin-4 (IL-4) levels were also ameliorated in mice treated with rifampicin. We next examined whether rifampicin has anti-atopic activity via suppression of mast cell activation. Rifampicin suppressed the release of ${\beta}$-hexosaminidase and histamine from human mast cell (HMC)-1 cultures stimulated with compound 48/80. Treatment with rifampicin also inhibited secretion of inflammatory mediators, such tumor necrosis factor-${\alpha}$ ($TNF-{\alpha}$) and prostaglandin $D_2$ ($PGD_2$), in mast cells activated by compound 48/80. The mRNA expression of cyclooxygenase 2 (COX-2) was reduced in the cells treated with rifampicin in a concentration-dependent manner. These results suggest that rifampicin can be used to treat atopic dermatitis.

• ALGAE
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• 제37권4호
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• pp.331-347
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• 2022

Atopic dermatitis (AD) is one of major skin inflammatory diseases characterized by excessive Th2-mediated immune responses. Recent evidence provides that interlukin-13 (IL-13) plays the role of a key Th2 cytokine that drives the inflammation underlining AD. Due to adverse effects of commercially available synthetic drugs, the need for treatments based on natural products is gaining much attention. Sargassum horneri is an edible brown algae known for beneficial bioactivities including anti-inflammation. We investigated if polyphenol-rich S. horneri extracts (SHE) could suppress AD-like skin lesions in NC/Nga mice and if that involved inhibition of the infiltration of Th2-mediated cytokine IL-13. We observed markedly increased infiltration of IL-13 positive cells in AD-like skin lesions of mice but SHE treatments decreased it. Also, the dermal expression of IL-13 was sufficient to cause inflammatory responses in mice skin resembling human AD. SHE suppressed the dermal infiltration of inflammatory cells where IL-13 plays a crucial role in skin tissues and in the recruitment of inflammatory cells. Furthermore, it was confirmed that SHE reduced T cell, dendritic cell, and macrophage populations in spleen. Moreover, SHE decreased the collagen deposition in skin and ear dermis resulting in reduced fibrosis that occurs in AD due to excessive collagen. Taken together, our results reveal that SHE suppressed the infiltration of inflammatory cells into skin dermis by decreasing the infiltration of IL-13 positive cells. Therefore, SHE could be taken as a useful therapeutic agent to alleviate AD.