表没食子儿茶素-3-没食子酸酯抑制烫伤诱导的小鼠皮肤巨噬细胞炎症蛋白-2的表达

李嘉雯 崔海燕 张东芳 肖鹏 李卫国*

doi:10.3969/j.issn.0529-1356.2013.03.007

解剖学报 ›› 2013, Vol. 44 ›› Issue (3) : 330-333. DOI: 10.3969/j.issn.0529-1356.2013.03.007

细胞和分子生物学

表没食子儿茶素-3-没食子酸酯抑制烫伤诱导的小鼠皮肤巨噬细胞炎症蛋白-2的表达

李嘉雯崔海燕张东芳肖鹏李卫国*

作者信息 +

Inhibition of epigallocatechin-3-gallate on scald-induced macrophage inflammatory protein-2 expression in the skin of mice

LI Jia-wen CUI Hai-yan ZHANG Dong-fang XIAO Peng LI Wei-guo*

Author information +

文章历史 +

摘要

目的探讨表没食子儿茶素-3-没食子酸酯(EGCG)对局部烫伤诱导的小鼠皮肤组织巨噬细胞炎症蛋白-2（MIP-2）表达的影响方法将
52只昆明种小鼠随机分为空白对照组、烫伤组和烫伤EGCG处理组，其中48只小鼠进行局部皮肤烫伤。利用实时定量PCR和ELISA法检测皮肤组织
MIP-2 mRNA和MIP-2蛋白水平。结果局部烫伤可引起受损部位皮肤组织的MIP-2 mRNA和MIP-2水平升高，而涂敷0.2g/kg EGCG膏剂可使MIP-2表
达水平下降。结论 0.2g/kg EGCG膏剂抑制局部烫伤诱导的皮肤组织MIP-2表达，减弱由MIP-2引起的炎症反应，促进受损皮肤修复。

Abstract

Objective To investigate influence of epigallocatechin-3-gallate (EGCG) on expression of macrophage inflammatory
protein-2(MIP-2) induced by locally scalded skin in mice. Methods Fity-two Kunming mice were divided into the control, scalded
skin, and EGCG groups. Forty-eight mice were used to establish a skin scalded model. The real time quantitative PCR (qRT-PCR)
and ELISA were used to evaluate MIP-2 expression in cutaneous tissue at both the mRNA and protein expression levels. Results
Both MIP-2 mRNA and protein levels in cutaneous tissue at injury sites increased after skin was scalded, but both decreased after
the scalded skin was treated by 0.2g/kg EGCG. Conclusion The data suggest that 0.2g/kg EGCG may suppress MIP-2 expression stimulated
by local skin scald, and decrease inflammatory reaction induced by MIP-2 release in cutaneous tissue at injury sites, thus EGCG
is able to promote the repair of skin injury elicited by scald.

导出引用

李嘉雯崔海燕张东芳肖鹏李卫国*. 表没食子儿茶素-3-没食子酸酯抑制烫伤诱导的小鼠皮肤巨噬细胞炎症蛋白-2的表达[J]. 解剖学报. 2013, 44(3): 330-333 https://doi.org/10.3969/j.issn.0529-1356.2013.03.007

LI Jia-wen CUI Hai-yan ZHANG Dong-fang XIAO Peng LI Wei-guo*. Inhibition of epigallocatechin-3-gallate on scald-induced macrophage inflammatory protein-2 expression in the skin of mice[J]. Acta Anatomica Sinica. 2013, 44(3): 330-333 https://doi.org/10.3969/j.issn.0529-1356.2013.03.007

中图分类号： Q249 Q786 R318

参考文献

［1］ Werner S, Grose R. Regulation of wound healing by growth factors and cytokines ［J］. Physiol Rev, 2003, 83(3):835-870.
［2］Burdon PCE, Martin C, Rankin SM. The CXC chemokine MIP-2 stimulates neutrophil mobilization from the rat bone marrow in a CD49d-dependent manner ［J］. Blood, 2005, 105(6):2543-2548.
［3］Bryan D, Walker KB, Ferguson M, et al. Cytokine gene expression in a murine wound healing model ［J］. Cytokine, 2005, 31(6):429-438.
［4］Park BK, Kim D, Cho S, et al. Effects of lipopolysaccharide and CpG-DNA on burn-induced skin injury ［J］. BMB Rep, 2011, 44(4):273-278.
［5］Babcock GF, Hernandez L, Yadav E, et al. The burn wound inflammatory response is influenced by midazolam ［J］. Inflammation, 2012, 35(1):259-270.
［6］Gauglitz GG, Song J, Herndon DN, et al. Characterization of the inflammatory response during acute and post-acute phases after severe burn ［J］. Shock, 2008, 30(5):503-507.
［7］Singh R, Akhtar N, Haqqi TM. Green tea polyphenol epigallocatechin-3-gallate: inflammation and arthritis ［J］. Life Sci, 2010, 86(25-26):907-918.
［8］ Zhang JJ, Jia YF, Li JW, et al. Epigallocatechin-3-gallate inhibits expression of tumor necrosis factor-α and interleukin-1β during skin scald repair in mice ［J］. Chinese Journal of Biochemistry and Molecular Biology, 2011, 27(2):168-173.（in Chinese）
张江江，贾永芳，李嘉雯，等. 表没食子儿茶素-3-没食子酸酯抑制TNF-α和IL-1β在小鼠皮肤烫伤修复期间的表达［J］.中国生物化学与分子生物学报,2011, 27(2):168-173. 
［9］Amulic B, Cazalet C, Hayes GL, et al. Neutrophil function: from mechanisms to disease ［J］. Annu Rev Immunol, 2012, 30:459-489.
［10］Skidgel RA, Gao XP, Brovkovych V, et al. Nitric oxide stimulates macrophage inflammatory protein-2 expression in sepsis ［J］. J Immunol, 2002, 169(4):2093-2101.
［11］Fournier BM, Parkos CA. The role of neutrophils during intestinal inflammation ［J］. Mucosal Immunol, 2012, 5(4):354-366.
［12］Bae HB, Li M, Kim JP, et al. The effect of epigallocatechin gallate on lipopolysaccharide- induced acute lung injury in a murine model［J］. Inflammation, 2010, 33(2):82-91.
［13］Tachibana H, Koga K, Fujimura Y, et al. A receptor for green tea polyphenol EGCG ［J］. Nat Struct Mol Biol, 2004, 11(4):380-381.
［14］Hong Byun E, Fujimura Y, Yamada K, et al. TLR4 signaling inhibitory pathway induced by green tea polyphenol epigallocatechin-3-gallate through 67-kDa laminin receptor［J］. J Immunol, 2010, 185(1):33-45.
［15］Byun EH, Omura T, Yamada K, et al. Green tea polyphenol epigallocatechin-3-gallate inhibits TLR2 signaling induced by peptidoglycan through the polyphenol sensing molecule 67-kDa laminin receptor ［J］. FEBS Lett, 2011, 585(5):814-820.