FIGURE 9.

A schematic diagram of the potential mechanisms by which ISOF treatment alleviates AECOPD in vivo. AECOPD model mice induced by cigarette smoke exposure and H1N1 virus infection have decreased lung function and increased pathological injury and inflammation, as well as activated NF-κB signaling and NLRP3 inflammasome and increased Th17 cells and IL-17A level in lung tissues. ISOF treatment attenuates the phosphorylation of NF-κB and the activation of NLRP3 inflammasome and decreases Th17 cells and IL-17A level in lung tissues, which could contribute to the decreased inflammatory response and improved lung function in AECOPD model mice. Thus, ISOF is a promising candidate for the prevention and treatment of AECOPD.