Cholesterol Accumulation Enhances Cigarette Smoke-Induced Airway Epithelial Inflammation.

Background: Statins, commonly used to lower cholesterol, have been shown to have anti-inflammatory effects in respiratory disease models. Disorders of cholesterol metabolism can cause damage to cells and tissues, and further lead to the development of a variety of diseases. However, the role of cholesterol metabolism in cigarette smoke-induced airway epithelial inflammation is unclear.

Inhibition of cathepsin L ameliorates inflammation through the A20/NF-κB pathway in endotoxin-induced acute lung injury.

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a severe inflammatory condition that remains refractory; however, its molecular mechanisms are largely unknown. Previous studies have shown numerous compounds containing 4-indolyl-2-aminopyrimidine that display strong anti-inflammatory properties. In our research, we identified that a 4-Indole-2-Arylaminopyrimidine derivative named "IAAP" suppressed lipopolysaccharide (LPS)-induced inflammation.