期刊文献+

(E)-苯乙基-3-(3,5-二羟基-4-异丙基苯基)丙烯酸酯对小鼠皮炎湿疹的治疗作用初步研究 被引量:5

The therapeutic effect of(E)-phenethyl 3-(3, 5-dihydroxy-4-isopropylphenyl) acrylate gels on dermatitis eczema in mice and the mechanism
下载PDF
导出
摘要 目的研究(E)-苯乙基-3-(3,5-二羟基-4-异丙基苯基)丙烯酸酯(THCA354)凝胶剂对小鼠变应性接触性皮炎(ACD)的治疗作用及机制。方法通过对小鼠耳廓涂抹2,4-二硝基氟苯(DNFB)诱导建立ACD模型,测定给予DNFB刺激后24 h的耳肿胀厚度和对小鼠耳组织进行病理组织形态学分析来共同评价THCA354凝胶剂的抗过敏作用效果;采用ELISA法和RT-PCR定量检测小鼠耳组织中炎症细胞因子含量及m RNA表达水平,初步阐明其作用机制。结果与阴性对照组相比,局部涂抹THCA354的小鼠耳肿胀程度、淋巴细胞浸润程度、耳组织匀浆中促炎细胞因子含量和m RNA表达水平均显著降低,抗炎细胞因子的含量和m RNA表达水平均显著升高。结论 THCA354可能是通过改变炎症细胞因子的分泌和m RNA表达水平,调节T细胞亚群的平衡从而发挥抗过敏作用。 The present study was designed to investigate the therapeutic effects of(E)-phenenthyl-3-(3,5-dihydroxy-4-isopropyl phenyl) acrylate gels(THCA354) on mouse allergic contactdermatitis(ACD) and toexplore the probable mechanisms. 1-fluoro-2, 4-dinitrobenzene(DNFB) was daubed on the ear of mice to induceACD model. Twenty-four hours after DNFB stimulation, by measuring the thickness of the ear and analyzing thehistopathologic morphology of ear tissue, we evaluate the anti-allergic effect of THCA354 gels. The protein andm RNA expression levels of inflammatory cytokines in mouse ear tissue homogenate were determined by ELISA andRT-PCR method. Compared with negative vehicle, the ear thickness, invasion degree of lymph cell and the proteinand m RNA levels of proinflammatory cytokine in ear tissue homogenate were significantly reduced, andanti-inflammatory cytokines were significantly raised in the group locally treated with THCA354 gel. In conclusion,THCA354 gels can exert anti-allergic effects by regulating the secretion and im RNA expression of inflammatorycytokines, thus to regulate the balance of the T cells subgroup.
出处 《免疫学杂志》 CAS CSCD 北大核心 2016年第4期299-304,共6页 Immunological Journal
关键词 THCA354凝胶剂 ACD模型 炎症细胞因子 m RNA表达水平 THCA354 gel ACD model Inflammatory cytokine m RNA expression level
  • 相关文献

参考文献2

二级参考文献31

  • 1郑敏.银屑病发病机制研究中若干问题的思考[J].中华皮肤科杂志,2006,39(3):121-123. 被引量:104
  • 2Kolls JK, Linden A. Interleukin-17 family members and inflammation [ J ]. Immunity, 2004, 21 (4) :467-476.
  • 3Ivanov II, Zhou L, Littman DR. Transcriptional regula- tion of Thl7 cell differentiation [ J]. Sere in Immunol, 2007, 9(6) :409-417.
  • 4Scholzen TE, Stander S, Riemann H, et al. Modulation of cutaneous inflammation by angiotensin- converting en- zyme[J]. J Immunol, 2003, 70(7): 3866-3873.
  • 5Ouyang W, Kolls JK, Zheng Y. The biological functions of T helper 17 cell effector cytokines in inflammation[ J]. Immunity, 2008,28 (4) : 454-467.
  • 6Larsen JM, Bonefeld CM, Poulsen SS, et al. IL-23 and Thl7-mediated inflammation in human allergic contact dermatitis[J]. J Allergy Clin Immunol, 2009,123(2), 486-492.
  • 7Nakae S, Komiyama Y, Nambu A, et al. Antigen-specif- ic T cell sensitization is impaired in IL-17-deficient mice, causing suppression of allergic cellular and humoral re- sponses[J]. Immunity, 2002, 17(3) :375-387.
  • 8Mitsui G, Mitsui K, Hirano T, et al. Kinetic profiles of sequential gene expressions for chemokines in mice with contact hypersensitivity [ J ]. Immunol Let, 2003, 86 (2) : 191-197.
  • 9Li K, Armstrong AW. A review of health outcomes in patients with psoriasis[J]. Dermatol Clin, 2012, 30(1): 61-72.
  • 10Neimann AL, Gelfand JM. The epidemiology of psoriasis[J]. Expert Rev Dermatol, 2006, 1(1): 63-75.

共引文献7

同被引文献42

引证文献5

二级引证文献45

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部