Piperlongumine reduces ovalbumin‑induced asthma and airway inflammation by regulating nuclear factor‑κB activation.

Asthma is a common chronic airway inflammatory disease, characterized by airway inflammation and remodeling. Piperlongumine (PL) has a number of physiological and pharmacological properties. However, the anti‑asthmatic effect of PL has not been reported to date. In the present study, ovalbumin (OVA) was used to sensitize and challenge mice to induce asthma. The results revealed that PL pretreatment reduced OVA‑induced airway inflammatory cell infiltration, reduced Th2 cytokine expression, both in the bronchoalveolar lavage fluid and in lung tissues, reduced the serum IgE level, pro‑inflammatory cytokine [tumor necrosis factor (TNF)‑α and interleukin (IL)‑6] and intercellular adhesion molecule expression, as well as nuclear factor (NF)‑κB activation. In addition, PL also mitigated OVA‑induced goblet cell metaplasia, inhibited mucus protein secretion, mitigated airway fibrosis and downregulated fibrosis marker expression. It was also demonstrated that PL inhibited TNF‑α induced inflammatory cytokine expression and NF‑κB activation in vitro. Taken together, the findings of the present study indicated that PL can reduce OVA‑induced airway inflammation and remodeling in asthmatic mice, and that these effects may be mediated by inhibiting NF‑κB signaling.