Schepens Eye Research Institute, and Massachusetts Eye and Ear Infirmary; and Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA.
Cornea. 2011 Dec;30(12):1465-72. doi: 10.1097/ICO.0b013e31821c9b5a.
To study the efficacy of topical epigallocatechin gallate (EGCG) for the treatment of dry eye disease (DED).
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-1β, tumor necrosis factor-α, 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.
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-1β (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.
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.
研究局部表没食子儿茶素没食子酸酯（EGCG）治疗干眼症（DED）的疗效。
将 7-8 周龄雌性 C57BL/6 小鼠饲养在受控环境室内以诱导 DED。将 0.01％或 0.1％EGCG 或载体局部应用于 DED 小鼠的眼睛。在不同组中评估角膜荧光素染色和角膜 CD11b+细胞的数量。通过实时聚合酶链反应评估第 9 天角膜中白细胞介素-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。用淋巴管内皮透明质酸受体（LYVE）-1 对角膜进行染色以评估淋巴管生成，并用末端转移酶 dUTP 缺口末端标记（TUNEL）试验评估角膜上皮细胞的凋亡。
与载体（24.6％，P=0.001）和未治疗对照组（41.9％，P<0.001）相比，用 0.1％EGCG 治疗显示角膜荧光素染色明显减少。与载体相比，在周边（23.3％，P=0.001）和中央（26.1％，P=0.009）角膜中，用 0.1％EGCG 治疗的眼睛中 CD11b+细胞的数量明显减少。与载体相比，用 0.1％EGCG 治疗与白细胞介素-1β（P=0.029）和趋化因子配体 2（P=0.001）的角膜表达降低相关，并且与未治疗组相比，VEGF-A 和 VEGF-D 水平降低（分别为 P=0.007 和 P=0.048）。0.01％EGCG 也显示在分子水平上炎症减轻，但 DED 的临床体征无明显变化。用 0.01％或 0.1％EGCG 处理未观察到对角膜上皮细胞的细胞毒性。
局部 EGCG 治疗通过抑制角膜中炎症细胞因子的表达和 CD11b+细胞的浸润，能够减轻 DED 的临床体征和炎症变化。
