Abstract
PurposeTo evaluate the safety and efficacy of Lycium barbarum polysaccharide (LBP) eye drops in a murine model of dry eye disease (DED).MethodsSix- to eight-week-old female C57BL/6 mice were subjected to a combination of desiccating stress (DS) and topical benzalkonium chloride (BAC) to induce DED. Five microliters of LBP eye drops (0.625, 2.5, or 12.5 mg/ml) or PBS was applied topically 3 times per day for 10 days to subsequently test their efficacy. Tear secretion, tear breakup time (TBUT), corneal irregularity, and corneal fluorescein staining scores were measured on days 3 and 10 after treatment. The expression of tumor necrosis factor-alpha (TNF-α) in the cornea was assessed by quantitative (q) RT–PCR on days 10. The ocular irritation of LBP eye drops of corresponding concentrations was evaluated on 10- to 12-week-old female Sprague–Dawley rats.ResultsCompared with PBS-treated groups, mice treated with 0.625, 2.5, and 12.5 mg/ml LBP showed a significant improvement in the clinical signs of DED in a dose-dependent manner, including corneal epithelial integrity, corneal regularity, and tear production, as well as significant inhibition of inflammatory cell infiltration and TNF-α expression levels in the cornea. All corresponding concentrations of LBP eye drops revealed no obvious ocular irritation.ConclusionTopical application of LBP could ameliorate dry eye in a murine model of DED without obvious ocular irritation.
Highlights
Dry eye disease (DED) is a chronic multifactorial ocular surface disease characterized by the loss of homeostasis of the tear film [1], affecting 5–50% of the population on a global scale [2]
We investigated the safety and efficacy of Lycium barbarum polysaccharide (LBP) eye drops in a murine model of DED and explored their potential mechanisms to provide primary data for LBP ophthalmic preparations
The corneal fluorescein staining scores significantly increased in the Desiccating stress (DS) + phosphate-buffered saline (PBS) group compared to the NS group 7 days after modeling [Figure 1B; NS vs. DS + PBS, 1.5 (2.25) vs. 12 (0.75), P < 0.0001]
Summary
Dry eye disease (DED) is a chronic multifactorial ocular surface disease characterized by the loss of homeostasis of the tear film [1], affecting 5–50% of the population on a global scale [2]. Ocular manifestations of DED include ocular discomfort, vision fluctuation, and potential damage to the ocular surface. The fundamental mechanism of DED is the vicious cycle caused by tear. Effects of LBP for DED film hyperosmolarity and ocular surface inflammation, in which mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) are the main signaling pathways [3]. Glucocorticoids, non-steroidal anti-inflammatory drugs (NSAIDs), and immunosuppressive agents are the most popular topical anti-inflammatory agents for DED [4]. Local and systemic side effects are relatively common and restrict their application in some cases [5–7]. Safe and effective DED treatments are under active exploration
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