Effects of erythromycin on γ‐glutamyl cysteine synthetase and interleukin‐1β in hyperoxia‐exposed lung tissue of premature newborn rats

Abstract

Objective: To explore the effect of erythromycin on hyperoxia‐induced lung injury. Methods: One‐day‐old preterm offspring Sprague‐Dawley (SD) rats were randomly divided into four groups: group 1, air + sodium chloride; group 2, air + erythromycin; group 3, hyperoxia + sodium chloride; and group 4, hyperoxia + erythromycin. At one, seven, and 14 days of exposure, glutathione (GSH) and interleukin‐1 beta (IL‐1 beta) were detected by double‐antibody sandwich enzyme‐linked immunosorbent assay (ELISA), and bicinchoninic acid (BCA) was used to detect GSH protein. γ‐glutamine‐cysteine synthetase (γ‐GCS) mRNA was detected by reverse transcription‐polymerase chain reaction (RT‐PCR). Results: Compared with group 1, expressions of GSH and γ‐GCS mRNA in group 3 were significantly increased at one and seven days of exposure (p < 0.05), but expression of γ‐GCS mRNA was significantly reduced at 14 days; expression of IL‐1 beta in group 3 was significantly increased at seven days of exposure (p < 0.05), and was significantly reduced at 14 days. Compared with group 3, expressions of GSH and γ‐GCS mRNA in group 4 were significantly increased at one, seven, and 14 days of exposure (p < 0.05), but expressions of GSH showed a downward trend at 14 days; expression of IL‐1 beta in group 4 was significantly reduced at one and seven days of exposure (p < 0.05). Conclusions: Changes in oxidant‐mediated IL‐1 beta and GSH are involved in the development of hyperoxia‐induced lung injury. Erythromycin may up‐regulate the activity of γ‐GCS, increasing the expression of GSH, inhibiting the levels of oxidant‐mediated IL‐1 beta and alleviating hyperoxia‐induced lung injury via an antioxidant effect.

Keywords

• Erythromycin
• Hyperoxia
• Lung injury
• Glutathione
• Interleukin‐1‐beta