2. Academic Validation
  3. Acetylshikonin alleviates pulmonary fibrosis through inhibition of the STAT3 signaling pathway

Acetylshikonin alleviates pulmonary fibrosis through inhibition of the STAT3 signaling pathway

  • Int Immunopharmacol. 2026 Jan 1;168(Pt 1):115811. doi: 10.1016/j.intimp.2025.115811.
Mengjie Qiu 1,  Jiayun Cheng 1,  Aofeng Sun 2,  Yi Zhou 3,  Chunbo Ma 2,  Yihan Ye 2,  Xiao Zhou 1,  Yini Xu 2,  Xiaofan Hong 4,  Chengguang Zhao 3,  Xinhu Wu 5,  Lehe Yang 6,  Haiyang Zhao 7
Affiliations

Affiliations

  • 1 Institute of Life Sciences, Biomedical Collaborative Innovation Center of Zhejiang Province, Wenzhou University, Wenzhou, Zhejiang 325035, China.
  • 2 The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 325000, China.
  • 3 School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.
  • 4 First School of Clinical Medicine, Wenzhou Medical University,Wenzhou, Zhejiang 325000, China.
  • 5 Affiliated Yueqing Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 325600, China. Electronic address: [email protected].
  • 6 The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 325000, China. Electronic address: [email protected].
  • 7 Institute of Life Sciences, Biomedical Collaborative Innovation Center of Zhejiang Province, Wenzhou University, Wenzhou, Zhejiang 325035, China. Electronic address: [email protected].
PMID: 41232362 DOI: 10.1016/j.intimp.2025.115811
Abstract

Pulmonary fibrosis (PF) is a refractory lung disease characterized by excessive extracellular matrix (ECM) deposition accompanied by inflammatory injury. Acetylshikonin (ASH), a naphthoquinone derivative primarily sourced from the root of Lithospermum erythrorhizon, possesses a diverse array of biological properties, including antitumor and anti-inflammatory activities, yet its potential in mitigating PF remains unexplored. We found that ASH ameliorated bleomycin-induced lung dysfunction and reduced lung inflammation levels, Collagen deposition and Epithelial-mesenchymal transition (EMT) in mice. ASH also inhibited the TGF-β1-induced increase in ECM deposition and EMT and inhibited the migration of cultured cells. Notably, ASH inhibited STAT3 phosphorylation and nuclear translocation, and overexpression of STAT3 in MLE-12 cells reversed the effects of ASH on ECM deposition and cell migration. Collectively, our studies demonstrate that ASH alleviates PF through inhibition of the STAT3 signaling pathway and provide compelling evidence that ASH is a promising candidate drug for the treatment of PF.

Keywords

Acetylshikonin; Bleomycin; EMT; Inhibition; Pulmonary fibrosis; STAT3.

Figures
Products
Inhibitors & Agonists
Other Products