Ginkgolide B protects human pulmonary alveolar epithelial A549 cells from lipopolysaccharide-induced inflammatory responses by reducing TRIM37-mediated NF-κB activation

The treatment options for acute stroke combined with pulmonary infection are limited. Clinically, there are several therapies to promote blood circulation and dissipate blood stasis; these treatment options include ginkgolide B (GB), which has PAF (platelet activating factor)-inhibiting effects. PAF-receptor (PAF-R) antagonists are used to treat a variety of inflammatory diseases; however, the potential of PAF-R antagonists as a treatment for lung infections remains unclear. The aim of the present study is to investigate the protective effect of GB on lipopolysaccharide-induced inflammatory responses in A549 human pulmonary alveolar epithelial cells (HPAEpiC) in vitro. Cell viability and apoptosis were measured by CCK-8 and flow cytometry. TRIM37, Caspase-3, and NF-kappa Bp65 expression levels were measured by real-time PCR and Western blotting. The release of tumor necrosis factor-alpha and interleukin-1 beta was measured by ELISA. The data indicates that GB may reduce TRIM37 expression by antagonizing the PAF-R pathway, thereby inhibiting the activation of nuclear factor-kappa B and alleviating the inflammatory response of alveolar epithelial cells. This study is the first to provide insight into the therapeutic potential of GB and suggests that clinical application of GB in acute stroke combined with pulmonary inflammation may be efficacious.