Knockdown of THBS1 inhibits inflammatory damage and oxidative stress in in vitro pneumonia model by regulating NF-κB signaling pathway.

Abstract

Pneumonia is an acute lower respiratory tract infection in children and the elderly. Recent studies have identified the significance of thrombospondin1 (THBS1) in inflammation. Nonetheless, the specific mechanisms by which THBS1 operates in pneumonia remain unclear. We treated 16HBE cells as an in vitro pneumonia model with lipopolysaccharide (LPS) and conducted a series of experiments to examine markers of inflammation and oxidative stress. LPS induces an increase in THBS1 expression in 16HBE cells. Knockdown of THBS1 reversed LPS-induced release of inflammatory factors [tumor necrosis factor α (TNF-α), interleukin (IL)-6, IL-1β]. Knocking down THBS1 reversed the LPS-induced increase in ROS and MDA and the decrease in SOD and GSH-Px. Inhibition of LPS led to the reversal of NF-κB pathway activation in response to LPS. Suppression of THBS1 hindered the NF-κB signaling cascade, resulting in a decrease in inflammation and oxidative stress triggered by LPS.