Investigational drug could be a potential treatment for dry-eye disease

By Paul Basilio, MDLinx
Published March 30, 2017

Key Takeaways

Edaravone, a drug approved in Japan to aid in neurological recovery following acute brain ischemia and subsequent cerebral infarction, could be a potential candidate for the treatment of hyperosmolarity-induced eye diseases.

An increase in tear osmolarity caused by increased evaporation of the aqueous tear phase has been considered a prominent pathological mechanism for dry-eye disease. Prior studies have shown that hyperosmolarity can cause inflammation of the ocular surface and can induce apoptosis in patients with dry eye.

Increased levels of reactive oxygen species (ROS), inflammatory cells, and lipid oxidative stress markers have been noted in the conjunctiva and tear film of patient’s with Sjögren’s syndrome. This suggests that oxidative stress plays a critical role in dry-eye disease.

In a study published in PLOS One, researchers found that edaravone partly reversed alterations in the generation of ROS and mitochondrial oxidative stress induced by hyperosmolarity. The drug also was noted to improve mitochondrial dysfunction and attenuated hyperosmolarity-induced cell death and apoptosis.

“With the exception of treatment for stroke,” the authors wrote, “the neuroprotective effects of edaravone have been verified in a number of diseases in which free radicals contribute to cell death, including both neurological and non-neurological diseases. However, reports on the protective effects of edaravone in dry eye disease are few. To the best of our knowledge, this is the first report to date on the protective effects of edaravone against hyperosmolarity-induced toxicity.”

Edaravone likely achieves this effect through the regulation of levels of ROS, mitochondrial function, and the expression of Nrf2, a protein that regulates the expression of antioxidant proteins that protect against oxidative damage triggered by injury and inflammation.

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