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- E-ISSN 2288-3339
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- P-ISSN1010-0695
- E-ISSN2288-3339
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Efficacy of Hataedock Treatments for Maintenance and Formation of Lipid Barrier in Obese NC/Nga Mice with Dermatophagoides Farinae-Induced Atopic Dermatitis
Journal of Korean Medicine / Journal of Korean Medicine, (P)1010-0695; (E)2288-3339
2018, v.39 no.4, pp.74-85
https://doi.org/10.13048/jkm.18036
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(2018). Efficacy of Hataedock Treatments for Maintenance and Formation of Lipid Barrier in Obese NC/Nga Mice with Dermatophagoides Farinae-Induced Atopic Dermatitis. Journal of Korean Medicine, 39(4), 74-85, https://doi.org/10.13048/jkm.18036
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Abstract
Objectives: HTD treatment is a traditional preventive therapy for neonatal inflammatory diseases such as AD. The aim of this study was to investigate the efficacy of HTD treatments for the maintenance and formation of lipid barrier in Dermatophagoides farina-induced obese NC/Nga mice. Methods: 20 mg/kg of CRGR extracts as HTD treatments were orally administered to NC/Nga mice. To induce obesity, high fat diet was served. Dermatophagoides farina extracts was applied on the 4th-6th and 8th-10th weeks to induce AD-like skin lesions in NC/Nga mice. Changes of skin conditions in mice were observed by histochemistry and immunohistochemistry. Results: The results showed that HTD treatments effectively maintained and formed the lipid barrier. In the experimental groups, restorations of Lass2 expression and distributions of filaggrin, involucrin, loricrin, ASM, and LXR means that HTD treatments maintained and generated the lipid barrier. In the dermal papillae, HTD treatments reduced PKC production accompanied by epidermis damage. Furthermore, levels of IL-4, and STAT6 was low. HTD treatment may be effective for preventing inflammation induced by Th2-skewed condition by suppressing the main pathway of Th2 differentiation. Conclusions: HTD treatment alleviated the inflammatory damage in the skin tissues of the NC/Nga mice by maintaining the lipid barrier and suppressing Th2 differentiation.
- keywords
- Hataedock, atopic dermatitis, NC/Nga obese mice, lipid barrier, Th2 differentiation
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