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http://dx.doi.org/10.13048/jkm.18036

Efficacy of Hataedock Treatments for Maintenance and Formation of Lipid Barrier in Obese NC/Nga Mice with Dermatophagoides Farinae-Induced Atopic Dermatitis  

Kim, Hee-Yeon (Department of Korean Pediatrics, School of Korean Medicine, Pusan National University)
Ahn, Sang-Hyun (Department of Anatomy, College of Korean Medicine, Semyung University)
Yang, In-Jun (Department of Physiology, College of Korean Medicine, Dongguk University)
Cheon, Jin-Hong (Department of Korean Pediatrics, School of Korean Medicine, Pusan National University)
Kim, Kibong (Department of Korean Pediatrics, School of Korean Medicine, Pusan National University)
Publication Information
The Journal of Korean Medicine / v.39, no.4, 2018 , pp. 74-85 More about this Journal
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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1 Hebenstreit D, Wirnsberger G, Horejs-Hoeck J, Duschl A. Signaling mechanisms, interaction partners, and target genes of STAT6. Cytokine Growth Factor Rev. 2006;17(3):173-88.   DOI
2 Shimoda K, van Deursen J, Sangster MY, Sarawar SR, Carson RT, Tripp RA, et al. Lack of IL-4-induced Th2 response and IgE class switching in mice with disrupted Stat6 gene. Nature. 1996;380(6575):630-3.   DOI
3 Mathew A, MacLean JA, DeHaan E, Tager AM, Green FH, Luster AD. Signal transducer and activator of transcription 6 controls chemokine production and T helper cell type 2 cell trafficking in allergic pulmonary inflammation. J Exp Med. 2001;193(9):1087-96.   DOI
4 Matsunaga MC, Yamauchi PS. IL-4 and IL-13 Inhibition in Atopic Dermatitis. J Drugs Dermatol. 2016;15(8):925-9.
5 Kopf M, Le Gros G, Bachmann M, Lamers MC, Bluethmann H, Kohler G. Disruption of the murine IL-4 gene blocks Th2 cytokine responses. Nature. 1993;362(6417):245-8.   DOI
6 Cornelissen C, Marquardt Y, Czaja K, Wenzel J, Frank J, Luscher-Firzlaff J, et al. IL-31 regulates differentiation and filaggrin expression in human organotypic skin models. J Allergy Clin Immunol. 2012;129(2):426-33.   DOI
7 Kim HJ, Shin JU, Lee KH. Atopic dermatitis and skin barrier dysfunction. Allergy Asthma Respir Dis. 2013;1(1):20-8.   DOI
8 Romieu I, Torrent M, Garcia-Esteban R, Ferrer C, Ribas-Fito N, Anto JM, et al. Maternal fish intake during pregnancy and atopy and asthma in infancy. Clin Exp Allergy. 2007;37(4):518-25.   DOI
9 Kim HY, Ahn SH, Yang IJ, Kim K. Effect of Skin Lipid Barrier Formation on Hataedock Treatment with Douchi. J Korean Med. 2017;38(2):41-52.   DOI
10 Jurakic Toncic R, Marinovic B. The Role of Impaired Epidermal Barrier Function in Atopic Dermatitis. Acta Dermatovenerol Croat. 2016;24(2):95-109.
11 Elias PM, Hatano Y, Williams ML. Basis for the barrier abnormality in atopic dermatitis: outside-inside-outside pathogenic mechanisms. J Allergy Clin Immunol. 2008;121(6):1337-43.   DOI
12 Thyssen JP, Kezic S. Causes of epidermal filaggrin reduction and their role in the pathogenesis of atopic dermatitis. J Allergy Clin Immunol. 2014;134(4):792-9.   DOI
13 Trayhurn P, Wood IS. Adipokines: inflammation and the pleiotropic role of white adipose tissue. Br J Nutr. 2004;92(3):347-55.   DOI
14 Bistrian BR, Khaodhiar L. Chronic systemic inflammation in overweight and obese adults. JAMA. 2000;283(17):2235.   DOI
15 Weisberg SP, McCann D. Desai M, Rosenbaum M, Leibel RL, Ferrante AW Jr.. Obesity is associated with macrophage accumulation in adipose tissue. J Clin Invest. 2003;112(12):1796-808.   DOI
16 Peng W, Novak N. Pathogenesis of atopic dermatitis. Clin Exp Allergy. 2015;45(3):566-74.   DOI
17 Kanchongkittiphon W, Gaffin JM, Phipatanakul W. Child with atopic dermatitis. Ann Allergy Asthma Immunol. 2015;114(1):6-11.   DOI
18 Kang KS. Nutritional Counseling for Obese Children with Obesity-Related Metabolic Abnormalities in Korea. Pediatr Gastroenterol Hepatol Nutr. 2017;20(2):71-8.   DOI
19 Silverberg JI, Kleiman E, Lev-Tov H, Silverberg NB, Durkin HG, Joks R, et al. Association between obesity and atopic dermatitis in childhood: A case-control study. J Allergy Clin Immunol. 2011;127(5):1180-6.   DOI
20 Mori S, Shiraishi A, Epplen K, Butcher D, Murase D, Yasuda Y, et al. Characterization of skin associated with obesity and specific correlation to local/systemic parameters in American women. Lipids Health Dis. 2017;16(1):214.   DOI
21 Kubo A, Nagao K, Amagai M. Epidermal barrier dysfunction and cutaneous sensitization in atopic diseases. J Clin Invest. 2012;122(2):440-7.   DOI
22 Elias PM. Lipid abnormalities and lipid-based repair strategies in atopic dermatitis. Biochim Biophys Acta. 2014;1841(3):323-30.   DOI
23 Taieb A. Hypothesis: from epidermal barrier dysfunction to atopic disorders. Contact Dermatitis. 1999;41(4):177-80.   DOI
24 Laviad EL, Albee L, Pankova-Kholmyansky I, Epstein S, Park H, Merrill AH, Jr., et al. Characterization of ceramide synthase 2: tissue distribution, substrate specificity, and inhibition by sphingosine 1-phosphate. J Biol Chem. 2008;283(9):5677-84.   DOI
25 Martin P, Villares R, Rodriguez-Mascarenhas S, Zaballos A, Leitges M, Kovac J, et al. Control of T helper 2 cell function and allergic airway inflammation by PKCzeta. Proc Natl Acad Sci U S A. 2005;102(28):9866-71.   DOI
26 Duran A, Rodriguez A, Martin P, Serrano M, Flores JM, Leitges M, et al. Crosstalk between PKCzeta and the IL4/Stat6 pathway during T-cell-mediated hepatitis. EMBO J. 2004;23(23):4595-605.   DOI
27 Benelli R, Lorusso G, Albini A, Noonan DM. Cytokines and chemokines as regulators of angiogenesis in health and disease. Curr Pharm Des. 2006;12(24):3101-15.   DOI
28 Charo IF, Taubman MB. Chemokines in the pathogenesis of vascular disease. Circ Res. 2004;95(9):858-66.   DOI
29 Holleran WM, Takagi Y, Uchida Y. Epidermal sphingolipids: metabolism, function, and roles in skin disorders. FEBS Lett. 2006;580(23):5456-66.   DOI
30 Li W, Sandhoff R, Kono M, Zerfas P, Hoffmann V, Ding BC, et al. Depletion of ceramides with very long chain fatty acids causes defective skin permeability barrier function, and neonatal lethality in ELOVL4 deficient mice. Int J Biol Sci. 2007;3(2):120-8.
31 Imokawa G, Abe A, Jin K, Higaki Y, Kawashima M, Hidano A. Decreased level of ceramides in stratum corneum of atopic dermatitis: an etiologic factor in atopic dry skin? J Invest Dermatol. 1991;96(4):523-6.   DOI
32 Janssens M, van Smeden J, Gooris GS, Bras W, Portale G, Caspers PJ, et al. Increase in short-chain ceramides correlates with an altered lipid organization and decreased barrier function in atopic eczema patients. J Lipid Res. 2012;53(12):2755-66.   DOI
33 O'Regan GM, Irvine AD. The role of filaggrin in the atopic diathesis. Clin Exp Allergy. 2010;40(7):965-72.   DOI
34 Schmuth M, Man MQ, Weber F, Gao W, Feingold KR, Fritsch P, et al. Permeability barrier disorder in Niemann-Pick disease: sphingomyelin-ceramide processing required for normal barrier homeostasis. J Invest Dermatol. 2000;115(3):459-66.   DOI
35 Denning MF. Epidermal keratinocytes: regulation of multiple cell phenotypes by multiple protein kinase C isoforms. Int J Biochem Cell Biol. 2004;36(7):1141-6.   DOI
36 Jung AR, Ahn SH, Park IS, Park SY, Jeong SI, Cheon JH, et al. Douchi (fermented Glycine max Merr.) alleviates atopic dermatitis-like skin lesions in NC/Nga mice by regulation of PKC and IL-4. BMC Complement Altern Med. 2016;16(1):416.   DOI
37 Kim H, Kim JR, Kang H, Choi J, Yang H, Lee P, et al. 7,8,4'-Trihydroxyisoflavone Attenuates DNCB-Induced Atopic Dermatitis-Like Symptoms in NC/Nga Mice. PLoS One. 2014;9(8): e104938.28.   DOI
38 Bao L, Mohan GC, Alexander JB, Doo C, Shen K, Bao J, et al. A molecular mechanism for IL-4 suppression of loricrin transcription in epidermal keratinocytes: implication for atopic dermatitis pathogenesis. Innate Immun. 2017;23(8):641-7.   DOI
39 Bao L, Alexander JB, Zhang H, Shen K, Chan LS. Interleukin-4 Downregulation of Involucrin Expression in Human Epidermal Keratinocytes Involves Stat6 Sequestration of the Coactivator CREB-Binding Protein. J Interferon Cytokine Res. 2016;36(6):374-81.   DOI
40 Steinert PM, Marekov LN. The proteins elafin, filaggrin, keratin intermediate filaments, loricrin, and small proline-rich proteins 1 and 2 are isodipeptide cross-linked components of the human epidermal cornified cell envelope. J Biol Chem. 1995;270(30):17702-11.   DOI
41 Pullmannova P, Stankova K, Pospisilova M, Skolova B, Zbytovska J, Vavrova K. Effects of sphingomyelin/ceramide ratio on the permeability and microstructure of model stratum corneum lipid membranes. Biochim Biophys Acta. 2014;1838(8):2115-26.   DOI
42 Di Nardo A, Wertz P, Giannetti A, Seidenari S. Ceramide and cholesterol composition of the skin of patients with atopic dermatitis. Acta Derm Venereol. 1998;78(1):27-30.   DOI
43 Hershey GK. IL-13 receptors and signaling pathways: an evolving web. J Allergy Clin Immunol. 2003;111(4):677-90.   DOI
44 Jensen JM, Folster-Holst R, Baranowsky A, Schunck M, Winoto-Morbach S, Neumann C, et al. Impaired sphingomyelinase activity and epidermal differentiation in atopic dermatitis. J Invest Dermatol. 2004;122(6):1423-31.   DOI
45 Man MQ, Choi EH, Schmuth M, Crumrine D, Uchida Y, Elias PM, et al. Basis for Improved Permeability Barrier Homeostasis Induced by PPAR and LXR Activators: Liposensors Stimulate Lipid Synthesis, Lamellar Body Secretion, and Post-Secretory Lipid Processing. J Invest Dermatol. 2006;126(2):386-92.   DOI
46 Delvecchio CJ, Capone JP. Protein kinase C alpha modulates liver X receptor alpha transactivation. J Endocrinol. 2008;197(1):121-30.   DOI
47 Schmuth M, Jiang YJ, Dubrac S, Elias PM, Feingold KR. Thematic review series: skin lipids. Peroxisome proliferator-activated receptors and liver X receptors in epidermal biology. J Lipid Res. 2008;49(3):499-509.   DOI
48 Walford HH, Doherty TA. STAT6 and lung inflammation. JAKSTAT. 2013;2(4):e25301.