Related Experiment Video
Updated: Aug 7, 2026
Analysis of the Ambient Particulate Matter-induced Chromosomal Aberrations Using an In Vitro System
Published on: December 21, 2016
Low-dose radiation mitigates PM2.5-induced lung impairment by down-regulating ROS-mediated inflammation and apoptotic
Rongrong Liu1, Yang Yu1, Zhiyuan Wang1
1NHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, China.
Background:
The adverse health effects of particulate matter 2.5 (PM2.5) have gained increasing recognition in recent years. Substantial evidence indicates that PM2.5 exposure contributes to the occurrence and progression of lung diseases, particularly through oxidative stress-mediated mechanisms involving inflammation and apoptosis. While low-dose radiation (LDR) has been extensively documented to attenuate inflammatory responses and apoptotic processes, its potential therapeutic efficacy in PM2.5-induced lung injury remains unclear. This study aims to investigate whether LDR intervention can mitigate lung damage associated with PM2.5 exposure.
Methods:
X-ray irradiation was used to develop mouse and cell models of PM2.5-induced lung damage. Transcriptomic profiling through RNA sequencing (RNA-seq) revealed differentially expressed genes associated with PM2.5 exposure. Inflammatory biomarkers in spleen, serum, and lung tissues were detected using flow cytometry, enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qRT-PCR), and Western blotting (WB) respectively. Concurrently, oxidative stress parameters and apoptotic markers in lung tissues and alveolar epithelial cells (A549 and MLE-12) were analyzed using biochemical assays, immunohistochemistry (IHC), and immunofluorescence (IF).
Results:
PM2.5 exposure significantly upregulated pro-inflammatory cytokines across all examined compartments, while LDR intervention substantially attenuated these inflammatory responses. Conversely, PM2.5 exposure significantly downregulated anti-inflammatory cytokines. In lung tissues, PM2.5 exposure significantly upregulated the expression of cytochrome c (Cyt c), caspase-3, and Bcl-2-associated X protein (Bax) compared to the control group. However, LDR treatment effectively attenuated these PM2.5-induced molecular alterations. Furthermore, A549 and MLE-12 cell lines were exposed to PM2.5 with or without LDR treatment. PM2.5 exposure significantly increased cellular apoptosis rates, while LDR treatment effectively attenuated this effect. The expression patterns of Cyt c, Bax, and caspase-3 in these cell lines exhibited consistent trends with those observed in pulmonary tissues. In addition, PM2.5 exposure significantly elevated oxidative stress markers, including malondialdehyde (MDA) content and cellular reactive oxygen species (ROS) production, while decreasing superoxide dismutase (SOD) levels. LDR treatment effectively attenuated these PM2.5-induced alterations. Notably, LDR demonstrated protective effects against PM2.5-induced mitochondrial integrity disruption.
Conclusions:
LDR mitigates PM2.5-induced lung damage primarily through the regulation of ROS-mediated inflammatory responses and apoptotic pathways.
