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<p>Acute lung injury (ALI) is a pathological condition characterised by varying degrees of lung damage in patients. Kirenol exerts anti-inflammatory, immunosuppressive, and antioxidative effects. We investigated the protective effects of kirenol on lipopolysaccharide-induced ALI in mice. Pretreatment with kirenol significantly ameliorated lung oedema and neutrophil infiltration in ALI mice. Kirenol downregulated the chemokines (MIP-2) expression and the adhesion molecules (ICAM-1 and VCAM-1) secretion. Furthermore, kirenol inhibited the production of the proinflammatory mediators nitric oxide and prostaglandin (PG)E2 through the upstream factors iNOS and cyclooxygenase (COX)-2, respectively. Kirenol suppressed the IKK-IκB-NFκB pathway, which is involved in lipopolysaccharide-induced inflammation. Kirenol inhibited the lipopolysaccharide-induced phosphorylation of ERK and JNK, to a lesser extent, p38 MAPK and Akt. In conclusion, our findings suggest that kirenol exerts ameliorative effects against ALI by suppressing the production of chemokines, adhesion molecules, and proinflammatory mediators and inhibiting the IKK-IκB-NFκB pathway and its upstream factors, phosphorylated ERK and JNK.</p>

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Kirenol ameliorates endotoxin-induced acute lung injury by inhibiting the ERK and JNK phosphorylation–mediated NFκB pathway in mice

  • 期刊论文

  • 发表日期：

    2025年3月4日

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  • Frank Cheau-Feng Lin,
  • Shih-Pin Chen,
  • Sheng-Chien Lin,
  • Ching-Chi Tseng,
  • Stella Chin-Shaw Tsai,
  • Yu-Hsiang Kuan

摘要

Acute lung injury (ALI) is a pathological condition characterised by varying degrees of lung damage in patients. Kirenol exerts anti-inflammatory, immunosuppressive, and antioxidative effects. We investigated the protective effects of kirenol on lipopolysaccharide-induced ALI in mice. Pretreatment with kirenol significantly ameliorated lung oedema and neutrophil infiltration in ALI mice. Kirenol downregulated the chemokines (MIP-2) expression and the adhesion molecules (ICAM-1 and VCAM-1) secretion. Furthermore, kirenol inhibited the production of the proinflammatory mediators nitric oxide and prostaglandin (PG)E2 through the upstream factors iNOS and cyclooxygenase (COX)-2, respectively. Kirenol suppressed the IKK-IκB-NFκB pathway, which is involved in lipopolysaccharide-induced inflammation. Kirenol inhibited the lipopolysaccharide-induced phosphorylation of ERK and JNK, to a lesser extent, p38 MAPK and Akt. In conclusion, our findings suggest that kirenol exerts ameliorative effects against ALI by suppressing the production of chemokines, adhesion molecules, and proinflammatory mediators and inhibiting the IKK-IκB-NFκB pathway and its upstream factors, phosphorylated ERK and JNK.