关键词： Infantile pneumonia Lipopolysaccharide (LPS) P300 RhoA/ROCK/NF-κB pathway

Mesh ： A549 Cells Cell Survival / drug effects physiology Down-Regulation / drug effects physiology E1A-Associated p300 Protein / antagonists & inhibitors metabolism Humans Inflammation / chemically induced metabolism Inflammation Mediators / antagonists & inhibitors metabolism Lipopolysaccharides / toxicity NF-kappa B / metabolism Signal Transduction / drug effects physiology rho-Associated Kinases / metabolism rhoA GTP-Binding Protein / metabolism

来  源：   DOI：10.1016/j.biopha.2017.10.104   PDF(Sci-hub)

Abstract：
Infantile pneumonia is a common disease in children, which affects cardiopulmonary function and even threats to life. Therefore, overall analysis about the mechanism of pathogenesis may be provided a new slight for the treatment of infantile pneumonia. This study aimed to investigate the role of p300 in lipopolysaccharide (LPS)-induced inflammatory injuries in A549 cells. MTT, flow cytometry, qRT-PCR and western blot assays were used to assess the effect of p300 on A549 cells viability, apoptosis and inflammatory cytokines expressions. Furthermore, RhoA/ROCK/NF-κB signaling pathways were analyzed by qRT-PCR and western blot. Results showed that p300 was significantly up-regulated in LPS-treated A549 cells. Knockdown of p300 promoted cell viability, inhibited apoptosis and decreased the expression levels of IL-1β, IL-6 and TNF-α in LPS-treated A549 cells. In addition, knockdown of p300 abolished the activation of the downstream RhoA/ROCK/NF-κB signaling pathways induced by LPS exposure via regulation of RhoA. In conclusion, p300 might be involved in progression of cell inflammatory response and could serve as a novel therapeutic target for clinical treatment of infantile pneumonia.
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