Comparative Effects of Flurbiprofen and Benzydamine on COX-2/PGE2 and Inflammatory Cytokine Release in Polyinosinic: polycytidylic Acid-Stimulated Human Tonsil and Bronchial Epithelial Cells

Topical non-steroidal anti-inflammatory drugs (NSAIDs) such as flurbiprofen and benzydamine may be used for the symptomatic relief of pharyngitis, triggered by infections. The onset and spectrum of anti-inflammatory activity of both drugs were compared in human tonsil (HTEpiC) and bronchial epithelial (BEAS-2B) cells stimulated with poly I:C against key inflammatory mediators. Cells were stimulated with poly I:C for 24 h and treated with flurbiprofen or benzydamine for 20 s, 2 min and 5 min. Production of prostaglandin E2 (PGE2), tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-1 beta (IL-1β), interleukin-8 (IL-8), interleukin-18 (IL-18), monocyte chemotactic protein-3 (MCP-3) and C-X-C motif chemokine ligand 10 (CXCL10), as well as cyclooxygenase-2 (COX-2) protein expression, was evaluated. Flurbiprofen significantly (p < 0.05) reduced PGE2 production and COX-2 expression in both cell types within 20 s of treatment and maintained these effects at 2 and 5 min. However, benzydamine produced delayed, inconsistent inhibition. Although both drugs reduced poly I:C induced IL-6, IL-1β, IL-8 and IL-18 production, the magnitude and onset were greater with flurbiprofen. Flurbiprofen also reduced MCP-3 and CXCL10 in both cell types, alongside significant inhibition of caspase-1 activity. Benzydamine showed limited or no effect and less inhibition of caspase-1. With rapid suppression of the COX-2/PGE2 pathway, rapid onset and a broad inhibition spectrum, flurbiprofen more comprehensively modulates inflammatory processes in epithelial respiratory models.