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Silica Promotes Silicosis via the ROS/NF-κB p65 Signaling-Activated Hypoxia-Lactate Axis in Rats
Yuan-Yuan Fu1, Yi-Fan Zhou2, Hui-Jie Hu1
1School of Public Health, Jining Medical University, Jining, Shandong, China.
Journal of Applied Toxicology : JAT
|April 21, 2026
Summary
Silica exposure causes lung hypoxia and damage by activating the ROS/NF-κB p65 pathway, leading to silicosis. N-acetylcysteine (NAC) treatment reversed these effects, highlighting a potential therapeutic target for this lung disease.
Area of Science:
- Pulmonary Medicine
- Toxicology
- Cellular Biology
Background:
- Silicosis is a progressive lung disease where hypoxia plays a role, but the exact mechanisms are unclear.
- Silica exposure is known to cause lung injury, inflammation, and fibrosis.
Purpose of the Study:
- To investigate the mechanisms by which silica induces hypoxia in silicosis.
- To explore the role of reactive oxygen species (ROS) and N-acetylcysteine (NAC) in silica-induced lung pathogenesis.
Main Methods:
- Fifty male rats were divided into control, silica-induced silicosis, and NAC-treated groups.
- Lung tissues were analyzed for histopathology and quantified for proteins involved in hypoxia (NF-κB p65, HIF-1α, VEGFA), lactate metabolism (GLUT1, LDHA), and inflammation (IL-1β, TGF-β1).
Main Results:
- Silica exposure led to lung damage, collagen deposition, and upregulation of hypoxia and inflammation markers compared to controls.
- NAC treatment dose-dependently reversed these silica-induced changes, indicating inhibition of ROS.
Conclusions:
- Silica induces pulmonary hypoxia via the ROS/NF-κB p65 pathway, triggering inflammation and fibrosis through lactic acid fermentation, ultimately causing silicosis.
- NAC demonstrates potential as a therapeutic agent by mitigating silica-induced lung injury.
