Downregulation of p300 alleviates LPS-induced inflammatory injuries through regulation of RhoA/ROCK/NF-κB pathways in A549 cells.

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.