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Tremella polysaccharides inhibit cellular apoptosis and autophagy induced by Pseudomonas aeruginosa lipopolysaccharide in A549 cells through sirtuin 1 activation
In the present study, the role of Tremella polysaccharides in cellular apoptosis and autophagy induced by Pseudomonas aeruginosa lipopolysaccharide (LPS) in human epithelial A549 lung-cancer cells was investigated. Initially, it was demonstrated that LPS attenuated A549 cell viability in a time- and...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5958729/ https://www.ncbi.nlm.nih.gov/pubmed/29805682 http://dx.doi.org/10.3892/ol.2018.8554 |
Sumario: | In the present study, the role of Tremella polysaccharides in cellular apoptosis and autophagy induced by Pseudomonas aeruginosa lipopolysaccharide (LPS) in human epithelial A549 lung-cancer cells was investigated. Initially, it was demonstrated that LPS attenuated A549 cell viability in a time- and dose-dependent manner. Furthermore, LPS induced apoptotic cell death and autophagy in A549 cells and increased reactive oxygen species (ROS) production in a time-dependent manner. In addition, LPS treatment was demonstrated to markedly suppress sirtuin 1 (SIRT1) protein expression in A549 cells. Notably, it was demonstrated that Tremella polysaccharides activate SIRT1, leading to increased p62 expression, decreased p53 acetylation and B-cell lymphoma 2-associated X protein expression, and subsequently attenuate LPS-induced apoptotic cell death and autophagy. The results of the present study demonstrated that Tremella polysaccharides activate SIRT1 and inhibit LPS-induced ROS production, apoptosis and autophagy. This may have critical implications for the treatment of Pseudomonas aeruginosa infection. |
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