ABSTRACT
OBJECTIVE: The aim of the present study is to investigate the effects of auraptene on inflammation and apoptosis of pneumonia cell model and uncover the mechanism. METHODS: WI-38 cells were treated with lipopolysaccharide (LPS) to construct a pneumonia model. Cell counting kit-8 assay, enzyme-linked-immunosorbent serologic assay, and quantitative polymerase chain reaction assay were conducted to confirm the effects of auraptene on the viability and inflammation of WI-38 cells. Flow cytometry (FCM) and immunoblot assays were conducted to detect the effects of auraptene on the apoptosis of WI-38 cells. Immunoblot assay was performed to confirm the mechanism. RESULTS: We found that auraptene stimulated cell viability in WI-38 cells upon LPS treatment. Auraptene also inhibited cellular inflammation. Furthermore, auraptene inhibited cell apoptosis of WI-38 cells upon LPS treatment. Mechanically, auraptene inhibited the nuclear factor kappa B signaling pathway, thereby suppressing the pneumonia. CONCLUSION: Auraptene alleviates inflammatory injury and cell apoptosis in pneumonia, thus has the potential to act as a pneumonia drug.
Subject(s)
MicroRNAs , Pneumonia , Humans , Child , Lipopolysaccharides/pharmacology , Pneumonia/drug therapy , Pneumonia/metabolism , Inflammation/drug therapy , Inflammation/metabolism , Apoptosis , MicroRNAs/metabolismABSTRACT
Objective: The aim of the present study is to investigate the effects of auraptene on inflammation and apoptosis of pneumonia cell model and uncover the mechanism. Methods: WI-38 cells were treated with lipopolysaccharide (LPS) to construct a pneumonia model. Cell counting kit-8 assay, enzyme-linked-immunosorbent serologic assay, and quantitative polymerase chain reaction assay were conducted to confirm the effects of auraptene on the viability and inflammation of WI-38 cells. Flow cytometry (FCM) and immunoblot assays were conducted to detect the effects of auraptene on the apoptosis of WI-38 cells. Immunoblot assay was performed to confirm the mechanism. Results: We found that auraptene stimulated cell viability in WI-38 cells upon LPS treatment. Auraptene also inhibited cellular inflammation. Furthermore, auraptene inhibited cell apoptosis of WI-38 cells upon LPS treatment. Mechanically, auraptene inhibited the nuclear factor kappa B signaling pathway, thereby suppressing the pneumonia. Conclusion: Auraptene alleviates inflammatory injury and cell apoptosis in pneumonia, thus has the potential to act as a pneumonia drug (AU)
