4.7 Article

Effects and mechanisms of aloperine on 2, 4-dinitrofluorobenzene-induced allergic contact dermatitis in BALB/c mice

期刊

EUROPEAN JOURNAL OF PHARMACOLOGY
卷 629, 期 1-3, 页码 147-152

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2009.12.007

关键词

Aloperine; Allergic contact dermatitis; Tumor necrosis factor-alpha; Interleukin-1 beta; Interleukin-6

资金

  1. Air Force General Hospital and Xinjiang Hope Pharmaceutical Company
  2. Institute of Psychology of Chinese Academy of Sciences [08CX043004]
  3. National Natural Science Foundation of China [30800301]
  4. Chinese Academy of Sciences [KSCX2-YW-R-254]

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Allergic contact dermatitis is a prototypic T-cell-mediated cutaneous inflammatory response. Multiple cell types, inflammatory mediators and cytokines are involved in the regulation of immunologic and inflammatory processes in allergic contact dermatitis. Aloperine is an isolated alkaloid found in the plant of Sophora alopecuroides L. It has been clinically proved effective in China for a long time for skin inflammatory diseases such as allergic contact dermatitis. However, the mechanism of aloperine on allergic contact dermatitis is largely unknown. Therefore, the aim of this study was to investigate the effect of aloperine on 2, 4-dinitrofluorobenzene (DNFB)-induced allergic contact dermatitis in BALB/c mice and the possible underlying mechanisms. The results showed that topical application of DNFB on the car provoked typical allergic contact dermatitis with ear swelling and ear erythema in BALB/c mice. Treatments with 1% aloperine suppressed DNFB-induced increase in ear thickness and ear erythema. Moreover, 1% aloperine treatment significantly decreased the up-regulated mRNA and protein levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) induced by DNFB in ear biopsy homogenates. Our findings suggest that aloperine greatly improves the DNFB-induced allergic contact dermatitis in mice. The therapeutic mechanism might be related to the reduction of TNF-alpha, IL-1 beta and IL-6 production induced by DNFB. (C) 2009 Elsevier B.V. All rights reserved.

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