Isoalantolactone alleviates ovalbumin‑induced asthmatic inflammation by reducing alternatively activated macrophage and STAT6/PPAR‑γ/KLF4 signals
Yunduan Song, Xiaozong Li, Fangfang Liu, Hongbo Zhu, Yao Shen
Abstract
Isoalantolactone (IAL), a sesquiterpene lactone, has anti‑inflammatory activity in lipopolysaccharide (LPS)‑induced sepsis. However, it remains to be elucidated whether IAL influences asthmatic inflammation. The present study found that IAL inhibited ovalbumin (OVA)‑induced asthmatic inflammation and attenuated OVA‑induced eosinophil infiltration, immunoglobulin E generation and the production of interleukin (IL)‑4, IL‑5, C‑C motif chemokine ligand (CCL)17 and CCL22. In addition, IAL treatment with IL‑4 reduced the expression of arginase‑1, Ym‑1, CCL17 and CCL22 in bone marrow‑derived macrophages <em>in vitro</em>. Furthermore, IAL inhibited IL‑4‑induced STAT6 phosphorylation and the expression of peroxisome proliferator‑activated receptor γ and Krüppel‑like factor 4. Collectively, the results suggested that IAL attenuated asthmatic inflammation and is a potential therapeutic agent for the treatment of asthma.