Open Access

ARTICLE

Taraxasterol Ameliorates Pulmonary Fibrosis by Regulating PPP2R1B Expression

Huiping Qiu¹, Shaofang Huang^2,*, Xin Xiong¹, Li Zhang¹

1 Department of Oncology, The Chest Hospital of Jiangxi Province, Nanchang, 330000, China
2 Department of Neurology, The Affiliated Hospital of Jiangxi University of Traditional Chinese Medicine, Nanchang, 330006, China

* Corresponding Author: Shaofang Huang. Email:

BIOCELL 2025, 49(12), 2415-2432. https://doi.org/10.32604/biocell.2025.070402

Received 15 July 2025; Accepted 13 October 2025; Issue published 24 December 2025

Abstract

Background: Pulmonary fibrosis is an irreversible lung disorder that currently has a limited number of effective therapeutic strategies. Taraxasterol (TAR), a bioactive triterpenoid isolated from plants used in traditional Chinese medicine (TCM), possesses anti-inflammatory and antioxidant activities. However, its precise role in pulmonary fibrosis remains incompletely defined. This study aimed to elucidate whether TAR alleviates pulmonary fibrosis by modulating Protein Phosphatase 2 Scaffold Subunit Abeta (PPP2R1B) expression. Methods: A bleomycin-induced murine model of pulmonary fibrosis and a transforming growth factor-β1 (TGF-β1) stimulated mouse lung fibroblast cell line (MLg) were established. To evaluate the effects of TAR on PPP2R1B expression and markers associated with fibrosis, histopathological staining, quantitative real-time PCR, Western blotting, and immunofluorescence were utilized. Additionally, si-PPP2R1B was used to validate its role in TAR-mediated anti-fibrotic effects. Results: 5 μg/mL TAR significantly suppressed 5 ng/mL TGF-β1-induced fibroblast activation, migration, and collagen deposition by downregulating PPP2R1B expression (p < 0.05). In vivo experiments demonstrated that 10 mg/kg TAR treatment improved alveolar structural integrity, reduced collagen accumulation, and suppressed the secretion of inflammatory cytokines (including TGF-β1, CTGF, TNF-α, and IL-1β) (p < 0.05). The concurrent improvement in these key histological and biochemical markers of pulmonary fibrosis indicates that TAR holds strong therapeutic potential for enhancing lung function. Furthermore, si-PPP2R1B confirmed the pivotal role of PPP2R1B in TAR anti-fibrotic action (p < 0.05). Conclusion: TAR ameliorates pulmonary fibrosis by downregulating PPP2R1B expression, which consequently attenuates TGF-β1-stimulated fibroblast activation, migration, and collagen deposition in vitro, and reduces collagen accumulation and inflammatory cytokine release in bleomycin-induced murine model of pulmonary fibrosis in vivo.

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