Protective effect of bromfenac sodium on femtosecond laser‑assisted cataract surgery via modulating cyclooxygenase‑2 expression

Cataract is a blinding‑caused disease and affects millions of individuals worldwide. Although conventional phacoemulsification (CPCS) has been widely used for treatment of cataract, the incidence of cataract‑caused blindness still increased year by year. Recently, femtosecond laser technology has been expanded to variety of clinical applications, including cataract surgery. The present study evaluated the curative effect of bromfenac sodium (BS) after femtosecond laser‑assisted cataract surgery (FLACS) and analyzed the mechanism of action. A total of 90 patients were randomly divided into five groups: Group I, conventional phacoemulsification treatment (CPCS) + dexamethasone (DEX)/tobramycin (TOB); group II, CPCS + bromfenac sodium (BS); group III, Femtosecond laser‑assisted cataract surgery (FLACS) + DEX/TOB; group IV, FLACS + BS; and group V, FLACS + pranoprofen. Aqueous humor was collected from these patients post‑surgery. For in vitro studies, SRA01/04 cells were irradiated using UV, followed by the collection of culture media and cell lysate. Prostaglandin E2 (PGE2) levels, an indicator of inflammation, were measured using ELISA both in vivo and in vitro. In addition, cyclooxygenase (COX) and cleaved caspase‑1 p20 expression levels were analyzed using western blotting. The findings suggested that BS was more effective and safer compared with glucocorticoids (GCs) after cataract surgery. BS can protect against post‑operative inflammation by inhibiting PGE2 production. Under in vitro conditions BS prevented the SRA01/04 cells from undergoing apoptosis after UV treatment and also suppressed PGE2 release from UV‑irradiated SRA01/04 cells by modulating COX‑2 expression. Furthermore, BS may have an inhibitory effect on the inflammatory form of cell death. Overall, these results indicated that BS could replace existing GCs as a reliable drug for a perioperative period of cataract surgery. It was also identified that the inhibitory effect of BS on PGE2 production was mediated via the regulation of COX‑2.