Burns : journal of the International Society for Burn Injuries · 2018
(-)-Epigallocatechin-3-gallate, reduces corneal damage secondary from experimental grade II alkali burns in mice.
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Gulias-Cañizo Rosario, Lagunes-Guillén Anell, González-Robles Arturo, Sánchez-Guzmán Erika, Castro-Muñozledo Federico
Аннотация
BACKGROUND: Since recent reports have shown that (-)-Epigallocatechin-3-gallate (EGCG) could be used for treating proliferative and inflammatory disorders, we explored its use for the management of corneal chemical burns.
MATERIALS AND METHODS: Initially, EGCG was assayed on the rabbit corneal epithelial cell line RCE1(5T5) to establish the best testing conditions, and to avoid unwanted outcomes in the experimental animals. Then, we studied its effects on cell proliferation, cell cycle progression and cell differentiation. Afterwards, we instilled EGCG in experimental grade II corneal alkali burns in mice, three times a day up to 21days, and evaluated by slit lamp examination and histological sections of corneal epithelial, corneal endothelial and stromal edema, as well as the presence of inflammatory cells and neovascularization.
RESULTS: EGCG reduced cell growth and led to a decline in the proportion of proliferative cells in a concentration dependent manner. At 10μM, EGCG promoted cell differentiation, an effect not related with apoptosis or cytotoxicity. When 10μM EGCG was instilled in corneal alkali burns in mice three times a day up to 21days, EGCG significantly reduced corneal opacity and neovascularization. The improved clinical appearance of the cornea was associated to a controlled epithelial growth; epithelial morphology was similar to that observed in normal epithelium and contrasted with the hyperproliferative, desquamating epithelium observed in control burn wounds. EGCG reduced corneal, stromal and endothelial edema, and wound inflammation.
CONCLUSION: This work constitutes the first evidence for the use of EGCG in the acute phase of a corneal alkali burn, representing a possible novel alternative to improve patient outcomes as an add-on therapy.
MATERIALS AND METHODS: Initially, EGCG was assayed on the rabbit corneal epithelial cell line RCE1(5T5) to establish the best testing conditions, and to avoid unwanted outcomes in the experimental animals. Then, we studied its effects on cell proliferation, cell cycle progression and cell differentiation. Afterwards, we instilled EGCG in experimental grade II corneal alkali burns in mice, three times a day up to 21days, and evaluated by slit lamp examination and histological sections of corneal epithelial, corneal endothelial and stromal edema, as well as the presence of inflammatory cells and neovascularization.
RESULTS: EGCG reduced cell growth and led to a decline in the proportion of proliferative cells in a concentration dependent manner. At 10μM, EGCG promoted cell differentiation, an effect not related with apoptosis or cytotoxicity. When 10μM EGCG was instilled in corneal alkali burns in mice three times a day up to 21days, EGCG significantly reduced corneal opacity and neovascularization. The improved clinical appearance of the cornea was associated to a controlled epithelial growth; epithelial morphology was similar to that observed in normal epithelium and contrasted with the hyperproliferative, desquamating epithelium observed in control burn wounds. EGCG reduced corneal, stromal and endothelial edema, and wound inflammation.
CONCLUSION: This work constitutes the first evidence for the use of EGCG in the acute phase of a corneal alkali burn, representing a possible novel alternative to improve patient outcomes as an add-on therapy.