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首页> 外文期刊>Cornea >Therapeutic efficacy of topical epigallocatechin gallate in murine dry eye.
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Therapeutic efficacy of topical epigallocatechin gallate in murine dry eye.

机译：局部表没食子儿茶素没食子酸酯在小鼠干眼中的治疗效果。

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OBJECTIVE: To study the efficacy of topical epigallocatechin gallate (EGCG) for the treatment of dry eye disease (DED). METHODS: Seven- to 8-week-old female C57BL/6 mice were housed in the controlled environment chamber to induce DED. Topical 0.01% or 0.1% EGCG, or vehicle, was applied to the eyes of DED mice. Corneal fluorescein staining and the number of corneal CD11b+ cells were assessed in the different groups. Expression of interleukin-1beta, tumor necrosis factor-alpha, chemokine ligand 2, and vascular endothelial growth factor (VEGF)-A/C/D was evaluated by real-time polymerase chain reaction in the corneas at day 9. Corneas were stained for lymphatic vessel endothelial hyaluronan receptor (LYVE)-1 to evaluate lymphangiogenesis, and the terminal transferase dUTP nick end labeling (TUNEL) assay was used to evaluate apoptosis of corneal epithelial cells. RESULTS: Treatment with 0.1% EGCG showed a significant decrease in corneal fluorescein staining compared with the vehicle (24.6%, P = 0.001) and untreated controls (41.9%, P < 0.001). A significant decrease in the number of CD11b+ cells was observed in 0.1% EGCG-treated eyes, compared with the vehicle in the peripheral (23.3%, P = 0.001) and central (26.1%, P = 0.009) corneas. Treatment with 0.1% EGCG was associated with a significant decrease in the corneal expression of interleukin-1beta (P = 0.029) and chemokine ligand 2 (P = 0.001) compared with the vehicle and in VEGF-A and VEGF-D levels compared with the untreated group (P = 0.007 and P = 0.048, respectively). EGCG 0.01% also showed a decrease in inflammation at the molecular level but no significant changes in the clinical signs of DED. No cellular toxicity to the corneal epithelium was observed with 0.01% or 0.1% EGCG. CONCLUSIONS: Topical EGCG treatment is able to reduce the clinical signs and inflammatory changes in DED by suppressing the inflammatory cytokine expression and infiltration of CD11b+ cells in the cornea.
机译：目的：研究表没食子儿茶素没食子酸酯没食子酸酯（EGCG）治疗干眼病（DED）的疗效。方法：将7至8周大的雌性C57BL / 6小鼠饲养在受控环境室内，诱导DED。将局部0.01％或0.1％的EGCG或赋形剂施用于DED小鼠的眼睛。在不同组中评估了角膜荧光素染色和角膜CD11b +细胞的数量。在第9天，通过实时聚合酶链反应评估白细胞介素-1β，肿瘤坏死因子-α，趋化因子配体2和血管内皮生长因子（VEGF）-A / C / D的表达。淋巴管内皮透明质酸受体（LYVE）-1评估淋巴管生成，终端转移酶dUTP缺口末端标记法（TUNEL）评估角膜上皮细胞凋亡。结果：与媒介物（24.6％，P = 0.001）和未处理的对照组（41.9％，P <0.001）相比，用0.1％EGCG处理的角膜荧光素染色显着降低。与周围（23.3％，P = 0.001）和中央（26.1％，P = 0.009）角膜中的媒介物相比，在0.1％EGCG处理的眼睛中观察到CD11b +细胞的数量显着减少。与媒介物相比，用0.1％EGCG处理与白介素，白细胞介素1β和趋化因子配体2的角膜表达（P = 0.029）和趋化因子配体2（P = 0.001）的显着降低有关，而与未经治疗的组（分别为P = 0.007和P = 0.048）。 EGCG 0.01％在分子水平上也显示炎症减少，但DED的临床体征无明显变化。用0.01％或0.1％的EGCG未观察到对角膜上皮的细胞毒性。结论：局部EGCG治疗能够通过抑制角膜中CD11b +细胞的炎性细胞因子表达和浸润来减少DED的临床体征和炎性变化。

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