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