Coenzyme Q10 alleviates silicotic fibrosis in rats through the TGF-β1/Smad pathway
Background: Silicosis, the most prevalent occupational disease worldwide, currently lacks effective clinical treatments. Therefore, identifying an effective intervention and preventive drug is crucial for inhibiting silicosis fibrosis. Our preliminary experiments suggested that coenzyme Q10 (CoQ10) may alleviate fibrosis in a rat silicosis model, but the underlying mechanism remains unclear. Methods: dust suspension. Rats were then treated with CoQ10 at doses of 20, 50, and 125 mg/kg/d to investigate its mechanism in improving silica-induced inflammation and fibrosis. Results: Results showed that CoQ10 significantly reduced levels of inflammatory cytokines IL-1β and TNF-α in bronchoalveolar lavage fluid (BALF), alleviated lung tissue inflammation, oxidative stress, and collagen deposition. In the medium- and high-dose CoQ10 groups, expression of fibrosis-related proteins (α-SMA, Vimentin, Col-I, Col-III) decreased, while E-cad expression increased. Moreover, expression of TGF-β1, Smad2, and Smad3 was downregulated, and Smad7 expression was upregulated. Conclusion: These findings suggest that the anti-fibrotic effect of CoQ10 on silicosis may be associated with reducing pulmonary inflammation and oxidative stress, thereby inhibiting the TGF-β1/Smad signaling pathway. This study provides new insights into understanding the pathogenesis and potential treatment of silicosis.
Authors
- Xiaofei Yang
- Jiping Yi
- Hongxiao Xie
- Tianci Xiong
- Lichao Zhan
- Hualing Zhang
- Yougen Wang
- Ming Zeng
Institutions
- Central South University (CN)
- Wuhan Prevention and Treatment Center for Occupational Diseases (CN)
- China Railway Group (China) (CN)
- Nanchang Center for Disease Control and Prevention (CN)
- University of South China (CN)
Publication Details
- Journal
- Frontiers in Pharmacology
- Published
- 2026-04-15
- DOI
- https://doi.org/10.3389/fphar.2026.1821205
- Primary Topic
- Coenzyme Q10 studies and effects
- Type
- article
- Field-Weighted Citation Impact
- 0.00