Conclusion
miR-135a-5p targeted TBK1 to regulate inflammatory/oxidative stress responses in ALI. Such results might bring a new potential target for ALI treatment.
Methods
MLE-12 cultures were treated with lipopolysaccharide (LPS) and transfected with miR-135a-5p mimics or TBK1 vector. An ALI mouse model was also established. Analysis was done on the relationships between TBK1 and miR-135a-5p. Inflammatory components, SOD, MDA, and ROS content were all assessed.
Objective
Acute inflammation and oxidative stress are present in large numbers in patients with acute lung injury (ALI). This investigation probed miR-135a-5p/TBK1 axis within ALI together with its new therapeutic target.
Results
Obvious inflammatory lesions were observed in lung tissues of ALI mice. Overexpression of miR-135a-5p or TBK1 knockdown remarkably decreased IL-1β, IL-6, and TNF-α serum concentrations and increased IL-10 level within lung tissues. Activated NRF2/TXNIP pathway and oxidative stress were additionally found within ALI murines, which were regulated by miR-315a-5p and TBK1. Further research revealed that miR-135a-5p negatively regulated TBK1 expression to mediate proinflammatory response and oxidative stress.