Deacetylforskolin ameliorates bleomycin-induced pulmonary fibrosis by suppressing inflammation and TGF-β1-induced epithelial-mesenchymal transition

doi:10.1007/s13659-026-00593-4

Natural Products and Bioprospecting ›› 2026, Vol. 16 ›› Issue (4): 52-52.DOI: 10.1007/s13659-026-00593-4

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Deacetylforskolin ameliorates bleomycin-induced pulmonary fibrosis by suppressing inflammation and TGF-β1-induced epithelial-mesenchymal transition

Yan Zhong^1,2, Chuang Xiao¹, Yaping Liang¹, Peng Wang¹, Yun Long¹, Shuyi Li¹, Na Song¹, Wenbin Shang¹, Weimin Yang¹, Xuan Zhang¹

1. School of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products/College of Modern Biomedical Industry, Kunming Medical University, Kunming 650500, China;
2. The People's Hospital of Dechang County, Liangshan Yi Autonomous Prefecture, Sichuan, 615500, China

Received:2025-11-22 Accepted:2026-01-06 Online:2026-08-29 Published:2026-08-22
Contact: Wenbin Shang,E-mail:shangwenbin@kmmu.edu.cn;Weimin Yang,E-mail:ywmbessie@yeah.net;Xuan Zhang,E-mail:zhangxuan@kmmu.edu.cn
Supported by:
This work was supported by the National Natural Science Foundation of China (No. 82460012, 82260727, 82560729, 22367018), the Basic Research Plan of Yunnan Provincial Science and Technology Department (No. 202101AY070001-010, 202301AY070001-175, 202401AT070173), First-Class Discipline Team of Kunming Medical University (2024XKTDTS13), Yunnan Key Laboratory of Pharmacology for Natural Products (YKLPNP-K2401), and the Yunnan Revitalization Talent Support Program (Chuang Xiao).

Deacetylforskolin ameliorates bleomycin-induced pulmonary fibrosis by suppressing inflammation and TGF-β1-induced epithelial-mesenchymal transition

Yan Zhong^1,2, Chuang Xiao¹, Yaping Liang¹, Peng Wang¹, Yun Long¹, Shuyi Li¹, Na Song¹, Wenbin Shang¹, Weimin Yang¹, Xuan Zhang¹

1. School of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products/College of Modern Biomedical Industry, Kunming Medical University, Kunming 650500, China;
2. The People's Hospital of Dechang County, Liangshan Yi Autonomous Prefecture, Sichuan, 615500, China

通讯作者: Wenbin Shang,E-mail:shangwenbin@kmmu.edu.cn;Weimin Yang,E-mail:ywmbessie@yeah.net;Xuan Zhang,E-mail:zhangxuan@kmmu.edu.cn
基金资助:
This work was supported by the National Natural Science Foundation of China (No. 82460012, 82260727, 82560729, 22367018), the Basic Research Plan of Yunnan Provincial Science and Technology Department (No. 202101AY070001-010, 202301AY070001-175, 202401AT070173), First-Class Discipline Team of Kunming Medical University (2024XKTDTS13), Yunnan Key Laboratory of Pharmacology for Natural Products (YKLPNP-K2401), and the Yunnan Revitalization Talent Support Program (Chuang Xiao).

Abstract

Abstract: Pulmonary fibrosis (PF) is a chronic, progressive and irreversible inflammatory disease with limited therapeutic methods in clinic. Deacetylforskolin (DFSK), derived from the plant Coleus forskohlii, is a potent adenylyl cyclase activator with potential anti-inflammatory activity. Herein, we attempted to investigate the therapeutic potential and mechanisms of DFSK against PF in bleomycin (BLM)-induced mouse models and TGF-β1-induced A549 cells. Our results showed that DFSK treatment alleviated lung injury and reduced inflammatory cytokines in a mouse model of BLM-induced acute lung inflammation, an early stage of PF. In a BLM-induced PF mouse model, DFSK attenuated pathological lung injury and collagen deposition, decreased pro-inflammatory cytokines (TNF-α, IL-1β) and profibrotic mediators (TGF-β1, CTGF, hydroxyproline). Upregulation of the epithelial marker E-cadherin and downregulation of the mesenchymal marker α-SMA were observed following DFSK treatment. Furthermore, DFSK significantly restored the pulmonary function of PF mice with decreased Te, f, Penh and increased RT, TV. Mechanistically, DFSK suppressed the phosphorylation of JNK and p38 MAPK, and inhibited TGF-β1-induced epithelial-mesenchymal transition (EMT) in A549 cells. Collectively, our findings demonstrate that DFSK is an effective therapeutic agent against PF by suppressing inflammation and EMT.

Key words: Pulmonary fibrosis, Deacetylforskolin, Inflammation, Epithelial–mesenchymal transition, MAPK signaling

摘要： Pulmonary fibrosis (PF) is a chronic, progressive and irreversible inflammatory disease with limited therapeutic methods in clinic. Deacetylforskolin (DFSK), derived from the plant Coleus forskohlii, is a potent adenylyl cyclase activator with potential anti-inflammatory activity. Herein, we attempted to investigate the therapeutic potential and mechanisms of DFSK against PF in bleomycin (BLM)-induced mouse models and TGF-β1-induced A549 cells. Our results showed that DFSK treatment alleviated lung injury and reduced inflammatory cytokines in a mouse model of BLM-induced acute lung inflammation, an early stage of PF. In a BLM-induced PF mouse model, DFSK attenuated pathological lung injury and collagen deposition, decreased pro-inflammatory cytokines (TNF-α, IL-1β) and profibrotic mediators (TGF-β1, CTGF, hydroxyproline). Upregulation of the epithelial marker E-cadherin and downregulation of the mesenchymal marker α-SMA were observed following DFSK treatment. Furthermore, DFSK significantly restored the pulmonary function of PF mice with decreased Te, f, Penh and increased RT, TV. Mechanistically, DFSK suppressed the phosphorylation of JNK and p38 MAPK, and inhibited TGF-β1-induced epithelial-mesenchymal transition (EMT) in A549 cells. Collectively, our findings demonstrate that DFSK is an effective therapeutic agent against PF by suppressing inflammation and EMT.

关键词: Pulmonary fibrosis, Deacetylforskolin, Inflammation, Epithelial–mesenchymal transition, MAPK signaling

Yan Zhong, Chuang Xiao, Yaping Liang, Peng Wang, Yun Long, Shuyi Li, Na Song, Wenbin Shang, Weimin Yang, Xuan Zhang. Deacetylforskolin ameliorates bleomycin-induced pulmonary fibrosis by suppressing inflammation and TGF-β1-induced epithelial-mesenchymal transition[J]. Natural Products and Bioprospecting, 2026, 16(4): 52-52.

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Deacetylforskolin ameliorates bleomycin-induced pulmonary fibrosis by suppressing inflammation and TGF-β1-induced epithelial-mesenchymal transition

Deacetylforskolin ameliorates bleomycin-induced pulmonary fibrosis by suppressing inflammation and TGF-β1-induced epithelial-mesenchymal transition

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