BACKGROUND/AIM: Human alveolar epithelial cells play a critical role in the pathogenesis of lung diseases. The objective of this study is to determine the contribution of beraprost sodium, a prostaglandin I2 (PGI2) analogue, to inflammatory and oxidative events in response to lipopolysaccharide (LPS) in airway epithelial cells. MATERIALS AND METHODS: Human pulmonary alveolar epithelial cells (A549) were pretreated with 10 µM beraprost sodium 30 min before stimulation with 1 µg/mL LPS for 24 h. The cellular viability assessments were evaluated by quantitative MTT test. Catalase activity and glutathione and lipid peroxidation levels were determined using spectrophotometric techniques. mRNA expression analyses were performed by real-time qRT-PCR. RESULTS: The endotoxin induced a dose-dependent increase in proliferation of the cells, which was suppressed by the beraprost sodium treatment. LPS increased the expressions of TNF-α and IL-1β genes by 8- and 2.5-fold, respectively. It also induced lipid peroxidation and depleted cellular antioxidant capacity. Pretreatments of the cells with beraprost sodium significantly reversed the inflammation and suppressed oxidative stress. CONCLUSION: These findings suggest that beraprost sodium will provide a pivotal molecular basis for the design of new therapeutic strategies to cure endotoxin-induced lung injury, although additional comprehensive studies are still required.
BACKGROUND/AIM: Human alveolar epithelial cells play a critical role in the pathogenesis of lung diseases. The objective of this study is to determine the contribution of beraprost sodium, a prostaglandin I2 (PGI2) analogue, to inflammatory and oxidative events in response to lipopolysaccharide (LPS) in airway epithelial cells. MATERIALS AND METHODS:Humanpulmonary alveolar epithelial cells (A549) were pretreated with 10 µM beraprost sodium 30 min before stimulation with 1 µg/mL LPS for 24 h. The cellular viability assessments were evaluated by quantitative MTT test. Catalase activity and glutathione and lipid peroxidation levels were determined using spectrophotometric techniques. mRNA expression analyses were performed by real-time qRT-PCR. RESULTS: The endotoxin induced a dose-dependent increase in proliferation of the cells, which was suppressed by the beraprost sodium treatment. LPS increased the expressions of TNF-α and IL-1β genes by 8- and 2.5-fold, respectively. It also induced lipid peroxidation and depleted cellular antioxidant capacity. Pretreatments of the cells with beraprost sodium significantly reversed the inflammation and suppressed oxidative stress. CONCLUSION: These findings suggest that beraprost sodium will provide a pivotal molecular basis for the design of new therapeutic strategies to cure endotoxin-induced lung injury, although additional comprehensive studies are still required.