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首页> 外文期刊>Nature reviews Cancer >Caffeic acid phenethyl ester attenuates nuclear factor-kappa B-mediated inflammatory responses in Muller cells and protects against retinal ganglion cell death
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Caffeic acid phenethyl ester attenuates nuclear factor-kappa B-mediated inflammatory responses in Muller cells and protects against retinal ganglion cell death

机译：咖啡酸苯乙烷衰减核因子-Kappa B介导的Muller细胞中的炎症反应，并防止视网膜神经节细胞死亡

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摘要

Glaucoma is characterized by the death of retinal ganglion cells (RGCs) and visual field defects, and is a leading cause of blindness worldwide. Caffeic acid phenethyl ester (CAPE), a natural polyphenolic found in propolis from honeybee hives, can inhibit the activation of nuclear factor kappa light-chain-enhancer of activated B cells (NF-kappa B) and has therapeutic potential in inflammatory disease. The present study used a rat model of optic nerve crush (ONC) injury to investigate the effect of CAPE on glaucoma. The death of RGCs at day 14 was significantly reduced in CAPE-treated animals compared with the non-treated group according to Brn3a and TUNEL staining. In addition, CAPE decreased the severity of inflammation in the retina, reflected by the decreased expression of inflammatory cytokines, including interleukin (IL)-8, IL-6, inducible nitric oxide synthase, cycloooxygenase-2, tumor necrosis factor-alpha and chemokine C-C ligand-2, in CAPE-treated rats. The hypertrophy of astrocytes and Muller cells (gliosis) caused by ONC was also found to be attenuated by CAPE, accompanied by the inhibition of NF-kappa B signaling. Similarly, in vitro, CAPE suppressed the proliferation and migration of primary astrocytes induced by lipopolysaccharide, as well as the activation of NF-kappa B. These results suggest that CAPE protected against RGC and attenuated inflammatory responses in a rat model of ONC by suppressing NF-kappa B activation.
机译：青光眼的特征是视网膜神经节细胞（RGC）和视野缺损的死亡，并且是全世界失明的主要原因。咖啡酸苯乙酯（CAPE），在从蜜蜂荨麻疹蜂胶中发现的天然多酚类，可以抑制核因子κB活化的B细胞（NF-κB的）的轻链增强子的激活，并且在炎症性疾病的治疗潜力。本研究中使用的视神经损伤（ONC）损伤的大鼠模型来研究CAPE对青光眼的影响。在第14天视网膜神经节细胞的死亡CAPE-治疗的动物显著降低与根据Brn3a和TUNEL染色非治疗组相比。另外，CAPE在视网膜减少炎症的严重性，反映了炎性细胞因子的表达下降，包括白细胞介素（IL）-8，IL-6，诱导型一氧化氮合酶，cycloooxygenase-2，肿瘤坏死因子-α和趋化因子CC配体2，在CAPE处理的大鼠。还发现星形细胞和造成ONC穆勒细胞（神经胶质增生）的肥大由CAPE衰减，伴随NF-κB信号的抑制。类似地，在体外，CAPE抑制增殖和脂多糖诱导原代星形胶质的迁移，以及NF-卡帕B的活化这些结果表明，CAPE保护，以防止RGC和通过抑制NF减弱ONC的大鼠模型中的炎症反应-κ乙活化。

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  • 来源
    《Nature reviews Cancer》 |2019年第6期|共9页
  • 作者

    Jia Yanwen; Jiang Shengqun; Chen Chen; Lu Guohua; Xie Yang; Sun Xincheng; Huang Liqin;

  • 作者单位

    Nanjing Med Univ Affiliated Changzhou Peoples Hosp 2 Eye Inst 29 Xinglong Lane Changzhou 213000;

    Bengbu Med Coll Affiliated Hosp 1 Dept Ophthalmol Bengbu 233000 Anhui Peoples R China;

    Nanjing Med Univ Affiliated Changzhou Peoples Hosp 2 Eye Inst 29 Xinglong Lane Changzhou 213000;

    Nanjing Med Univ Affiliated Changzhou Peoples Hosp 2 Eye Inst 29 Xinglong Lane Changzhou 213000;

    Nanjing Med Univ Affiliated Changzhou Peoples Hosp 2 Eye Inst 29 Xinglong Lane Changzhou 213000;

    Nanjing Med Univ Affiliated Changzhou Peoples Hosp 2 Eye Inst 29 Xinglong Lane Changzhou 213000;

    Nanjing Med Univ Affiliated Changzhou Peoples Hosp 2 Eye Inst 29 Xinglong Lane Changzhou 213000;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 肿瘤学;
  • 关键词

    caffeic acid phenethyl ester; NF-kappa B; inflammatory responses; Muller cells; retinal ganglion cell;

    机译：咖啡酸苯乙烷酯;nf-κB;炎症反应;瘤瘤细胞;视网膜神经节细胞;

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