Benzydamine reduces prostaglandin production in human gingival fibroblasts challenged with interleukin-1β or tumor necrosis factor α

Benzydamine [1-benzyl-3-(3-dimethylamino)propoxy-1H-indazole] is a drug with, analgesic, anesthetic, antimicrobial and anti-inflammatory activity. The purpose of the present study was to investigate the effect of benzydamine on prostaglandin production in human gingival fibroblasts. Benzydamine significantly reduced the basal production of both prostaglandin E-2 (PGE(2)) and 6-keto-PGF(1 alpha), the stable breakdown product of prostaglandin I-2(PGI(2)), in unstimulated human gingival fibroblasts. When the cells were treated simultaneously with benzydamine and the cytokines IL-1 beta or TNF alpha, the agent benzydamine reduced (P < 0.05) the stimulatori effect of IL-1 beta and TNF alpha respectively, on PGE(2) and PGI(2) production in human gingival fibroblasts. Furthermore, benzydamine reduced (P < 0.05) both the basal level and the cytokine induced H-3-arachidonic acid release H-3-(AA) in gingival fibroblasts. The addition of exogenous arachidonic acid to the cells resulted in enhanced PGE(2) production, which was reduced (P < 0.05) in the presence of benzydamine. The study indicates that benzydamine reduces che prostaglandin synthesis in gingival fibroblasts, partly at the level of phospholipase A(2), by diminishing the liberation of arachidonic acid (AA) from phospholipids, and partly at the level of cyclooxygenase. The inhibitory effect of benzydamine on prostaglandin production may explain the anti-inflammatory effect of the drug in the management of patients with oral inflammatory conditions.