Protective Effects ofProtein Hydrolysate against Atropine-Induced Dry Eye Disease.

Abstract

Dry eye disease (DED) is a multifactorial ocular disorder characterized by tear film instability, inflammation, and ocular surface damage. Although various therapeutic approaches are available, there remains a strong need for safer and more effective agents with clearly defined mechanisms of action. This study examined the protective effects ofprotein hydrolysate (MMH) in bothandmodels of DED., pretreatment of air-dried human corneal epithelial cells with MMH attenuated oxidative stress and apoptosis., oral administration of MMH to rats with atropine-induced DED restored tear secretion, preserved ocular tissue architecture, reduced immune cell infiltration, and downregulated inflammatory mediators in the cornea. Furthermore, MMH maintained tight junction proteins, suppressed pro-apoptotic signaling in the lacrimal gland, improved meibomian gland and goblet cell integrity, and mitigated neovascularization. Collectively, MMH demonstrated anti-inflammatory, anti-apoptotic, and tissue-protective effects, supporting its potential as a novel therapeutic candidate for DED.