Obtusifolin ameliorates dry eye model in rats by reducing inflammation and blocking MAPK/NF-κB pathways

Obtusifolin ameliorates dry eye model in rats by reducing inflammation and blocking MAPK/NF-κB pathways

AIM: To investigate the functions and potential mechanisms of obtusifolin in dry eye disease (DED) in a rat model. METHODS: A rat DED model was established via topical administration of benzalkonium chloride (BAC), followed by administration of obtusifolin. Conjunctival irritation score and tear pro...

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Bibliographic Details
Main Authors: Dan Zhu, Xiao-Yang Wu, Liang-Chang Li
Format: Article
Language:English
Published: Press of International Journal of Ophthalmology (IJO PRESS) 2025-08-01
Series:International Journal of Ophthalmology
Subjects:
dry eye disease
obtusifolin
inflammation
tear production
mitogen-activated protein kinase/nuclear factor kappa b
rats
Online Access:http://ies.ijo.cn/en_publish/2025/8/20250802.pdf
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Summary:AIM: To investigate the functions and potential mechanisms of obtusifolin in dry eye disease (DED) in a rat model. METHODS: A rat DED model was established via topical administration of benzalkonium chloride (BAC), followed by administration of obtusifolin. Conjunctival irritation score and tear production were measured to evaluate DED symptoms. Enzyme-linked immunosorbent assay (ELISA) was employed for determining inflammatory cytokine levels in rat conjunctiva. Periodic acid-Schiff staining and corneal fluorescein staining were implemented for assessing goblet cell numbers and corneal epithelial defects, respectively. Western blotting showed zonula occludens-1 (ZO-1), matrix metalloproteinase-9 (MMP-9), and mitogen-activated protein kinase (MAPK)/nuclear factor kappa B (NF-κB) signaling-related protein levels in the conjunctiva. RESULTS: Topical application of obtusifolin alleviated conjunctival irritation and enhanced tear production in BAC-induced DED rats. Obtusifolin attenuated conjunctival inflammatory response and goblet cell loss as well as corneal epithelial barrier disruption in DED rats. Obtusifolin suppressed extracellular signal-regulated kinase (ERK), p38, and NF-κB phosphorylation in the conjunctiva of DED rats. CONCLUSION: Obtusifolin ameliorates DED in rats possibly by alleviating inflammation via the inactivation of MAPK/NF-κB signaling.
ISSN:2222-3959
2227-4898

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