Protective Effects of <i>Misgurnus mizolepis</i> Protein Hydrolysate against Atropine-Induced Dry Eye Disease

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 of <i>Misgurnus mizolepis</i> protein hydrolysate (MMH) in both <i>in vitro</i> and <i>in vivo</i> models of DED. <i>In vitro</i>, pretreatment of air-dried human corneal epithelial cells with MMH attenuated oxidative stress and apoptosis. <i>In vivo</i>, 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.