十二烷基硫酸钠诱导银屑病动物模型的建立

张海婧,周琬琪,张 翼,金 晶,陈晓光

武警医学 ›› 2013, Vol. 24 ›› Issue (5) : 373-375.

武警医学 ›› 2013, Vol. 24 ›› Issue (5) : 373-375.
论著

十二烷基硫酸钠诱导银屑病动物模型的建立

  • 张海婧,周琬琪,张 翼,金 晶,陈晓光
作者信息 +

Establishment of a psoriasis animal model using SDS

  • ZHANG Haijing,ZHOU Wanqi,ZHANG Yi,JIN Jing,and CHEN Xiaoguang.
Author information +
文章历史 +

摘要

目的 建立一种简单、快速筛选银屑病治疗药物的模型。方法 应用10%十二烷基硫酸钠(sodium dodecyl sulfate, SDS)涂抹模型组小鼠背部皮肤,对照组小鼠涂抹蒸馏水,观察两组皮肤组织的改变。结果 经过10% SDS涂抹7 d后的模型组小鼠皮肤可见明显银屑病样体征,如皮肤增厚[(0.87±0.33) mm vs (0.60±0.02) mm]、红肿和皮下血管增生等。病理检测证明模型组小鼠皮肤出现角化过度和角质层增厚,真皮层和皮下层可见毛细血管扩张和充血等银屑病样改变。Western-blot结果证明,血清中的PKCβ、IL-1 β、TNF-α、IL-23等细胞因子表达上调。结果显示SDS所诱导的小鼠模型能够反映银屑病的某些特征。结论 利用10%SDS涂抹小鼠皮肤可建立银屑病动物模型,方法简单、快速。

Abstract

Objective To establish a simple, rapid psoriasis model. Methods 10% SDS was applied to the skin of test group ,while distilled water was applied to the skin of control group. Results After 10% SDS was applied for 7 d, psoriasis symptoms were produced on skin of test mice such as skin thickening, swelling and subcutaneous vascular proliferation, etc. Pathology detected hyperkeratosis and corneous layer thickening, visible blood capillary dilation and congestion in the dermis and subcutaneous layer of test mice skin, compared with control mice skin. Western blotting results showed expressions of PKC β, IL - 1 β, TNF alpha, and IL - 23 were upregulated. The results above showed that the SDS-induced mouse model could reflect the some characteristics of psoriasis. Conclusions A simple, rapid psoriasis animal model is established using 10% SDS.

关键词

银屑病 / 动物模型 / 十二烷基硫酸钠

Key words

psoriasis / animal model / SDS

引用本文

导出引用
张海婧,周琬琪,张 翼,金 晶,陈晓光. 十二烷基硫酸钠诱导银屑病动物模型的建立[J]. 武警医学. 2013, 24(5): 373-375
ZHANG Haijing,ZHOU Wanqi,ZHANG Yi,JIN Jing,and CHEN Xiaoguang.. Establishment of a psoriasis animal model using SDS[J]. Medical Journal of the Chinese People Armed Police Forces. 2013, 24(5): 373-375
中图分类号: R332   

参考文献

[1] Bowcock A M, Cookson W O. The genetics of psoriasis, psoriatic arthritis and atopic dermatitis[J]. Hum Mol Genet , 2004,13 (1):43-55.

[2] Mak R K, Hundhausen C, Nestle F O. Progress in understanding the immunopathogenesis of psoriasis[J]. Actas Dermosifiliogr, 2009,100:2-13.

[3] Martínez-Santamaría L, Guerrero-Aspizua S, Del Río M.Skin bioengineering: preclinical and clinical applications [J].Actas Dermosifiliogr, 2012,103(1):5-11.

[4] Wagner E F, Schonthaler H B, Guinea-Viniegra J, et al. Psoriasis: what we have learned from mouse models[J]. Nat Rev Rheumatol, 2010,6(12):704-714.

[5] Danilenko D M. Review paper: preclinical models of psoriasis [J]. Vet Pathol, 2008, 45(4):563-575.

[6] Schön M P. Animal models of psoriasis: a critical appraisal[J].Exp Dermatol, 2008,17(8):703-712.

[7] De Smedt A C, Van Den Heuvel R L, Zwi Berneman N,et al.Modulation of phenotype, cytokine production and stimulatory function of CD34+-derived DC by NiCl(2) and SDS[J].Toxicol In Vitro, 2001,15(4-5):319-325.

[8] Rougier N, Redziniak G, Mougin D, et al. In vitro evaluation of the sensitization potential of weak contact allergens using langerhans-like dendritic cells and autologous T cells[J].Toxicology, 2000, 145(1):73-82.

[9] Rachael A C, Kupper T S. Misbehaving macrophages in the pathogenesis of psoriasis[J]. J Clin Invest, 2006, 116(8): 2084–2087.

[10] Van de, Kerkhof P C. The evolution of the psoriatic lesion[J].Br J Dermatol, 2007,157(1):4-15.

[11] Mabuchi T, Chang T W, Quinter S, et al. Chemokine receptors in the pathogenesis and therapy of psoriasis[J].J Dermatol Sci, 2012, 65(1):4-11.

[12] Ayroldi E, Bastianelli A, Cannarile L, et al. A pathogenetic approach to autoimmune skin disease therapy: psoriasis and biological drugs, unresolved issues, and future directions [J].Curr Pharm Des, 2011,17(29):3176-3190.

[13] Rozieres A, Hennino A, Nicolas J F. TNF alpha in the physiopathology of psoriasis[J].Ann Dermatol Venereol, 2006,133(2):174-180.

[14] Maioli E, Valacchi G.Rottlerin: bases for a possible usage in psoriasis[J]. Curr Drug Metab, 2010,11(5):425-430.

[15] Manicassamy S.Sotrastaurin, a protein kinase C inhibitor for the prevention of transplant rejection and treatment of psoriasis[J]. Curr Opin Investig Drugs, 2009,10(11): 1225-1235.

[16] Tortola L, Rosenwald E, Abel B, et al. Psoriasiform dermatitis is driven by IL-36-mediated DC-keratinocyte crosstalk[J]. J Clin Invest, 2012,122(11):3965-3976.

[17] Johnson-Huang L M, McNutt N S, Krueger J G, et al.Cytokine-producing dendritic cells in the pathogenesis of inflammatory skin diseases[J].J Clin Immunol, 2009,29(3):247-256.

[18] Zaba L C, Fuentes D J, Eungdamrong N J, et al.Psoriasis is characterized by accumulation of immunostimulatory and Th1/Th17 cell-polarizing myeloid dendritic cells[J].J Invest Dermatol, 2009,129(1):79-88.

基金

国家自然科学基金青年基金项目(81001443)


Accesses

Citation

Detail

段落导航
相关文章

/