Matrine Reduces Intraocular Pressure in Corticosteroid-Induced Ocular Hypertensive Mouse Eyes.
Qi Zhang, Zhiquan Liu, Siyu Chen, Qing Wang, Chien-Hui Lo, Ke Ning, Jingyu Zhao, Yingchun Shen, Paloma B Liton, Yang Sun
Summary
Matrine decreased the IOP in the DEX-induced OHT mouse model, highlighting its potential as a therapeutic agent for managing glaucoma, particularly in corticosteroid-associated secondary cases.
Abstract
PURPOSE
This study investigates the potential of matrine, a quinolizidine alkaloid, in regulating intraocular pressure (IOP) in normal and corticosteroid-induced ocular hypertension (OHT) mice.
METHODS
Wild-type C57BL/6 mice were randomly divided into normal and OHT groups. The OHT mouse model was established by periocular conjunctival fornix injections of dexamethasone-21-acetate (DEX). IOP was measured at 0.0, 0.5, 1.0, 3.0, and 6.0 hours after matrine treatment in both groups. Aqueous humor (AH) outflow facility was measured using our previously described/validated perfusion system. Anterior segment-optical coherence tomography was used to evaluate morphological changes in the anterior chamber following matrine treatment. Hematoxylin and eosin staining and immunofluorescence staining were used to investigate structural changes.
RESULTS
Matrine treatment (50-200 µg/g) decreased the IOP in normal mice in a dose-dependent manner. AH outflow facility in normal mice elevated at 0.5 hours after matrine treatment (100 and 200 µg/g). Additionally, 100 µg/g matrine treatment increased the angle opening distance in the anterior chamber. In DEX-induced OHT mice, matrine (100 and 200 µg/g) reduced the elevated IOP and increased the AH outflow facility. Furthermore, 100 µg/g matrine treatment increased the angle opening distance compared with that of PBS-treated controls. However, matrine (100 µg/g) did not induce significant changes in trabecular meshwork gross morphology or the expression of cell contractility and extracellular matrix markers in OHT mice at 0.5 hours after treatment.
CONCLUSIONS
Matrine decreased the IOP in the DEX-induced OHT mouse model, highlighting its potential as a therapeutic agent for managing glaucoma, particularly in corticosteroid-associated secondary cases.
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