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Lias overexpression alleviates pulmonary injury induced by fine particulate matter in mice
Guangcui Xu1, Yingzheng Zhao1, Yingjun Tao1
1School of Public Health, Xinxiang Medical University, Xinxiang, 453003, Henan, People's Republic of China.
Abstract:
Oxidative stress and inflammation are mechanisms underlying toxicity induced by fine particulate matter (PM2.5). The antioxidant baseline of the human body modulates the intensity of oxidative stress in vivo. This present study aimed to evaluate the role of endogenous antioxidants in alleviating PM2.5-induced pulmonary injury using a novel mouse model (LiasH/H) with an endogenous antioxidant capacity of approximately 150% of its wild-type counterpart (Lias+/+). LiasH/H and wild-type (Lias+/+) mice were randomly divided into control and PM2.5 exposure groups (n = 10), respectively. Mice in the PM2.5 group and the control group were intratracheally instilled with PM2.5 suspension and saline, respectively, once a day for 7 consecutive days. The metal content, major pathological changes in the lung, and levels of oxidative stress and inflammation biomarkers were examined. The results showed that PM2.5 exposure induced oxidative stress in mice. Overexpression of the Lias gene significantly increased the antioxidant levels and decreased inflammatory responses induced by PM2.5. Further study found that LiasH/H mice exerted their antioxidant function by activating the ROS-p38MAPK-Nrf2 pathway. Therefore, the novel mouse model is useful for the elucidation of the mechanisms of pulmonary injury induced by PM2.5.
Insights
Enhanced antioxidant capacity in mice reduced lung injury from fine particulate matter (PM2.5). This study highlights the protective role of endogenous antioxidants against PM2.5-induced oxidative stress and inflammation.
Area of Science:
- Environmental Health
- Toxicology
- Molecular Biology
Background:
- Fine particulate matter (PM2.5) exposure is a significant environmental health concern, linked to pulmonary toxicity via oxidative stress and inflammation.
- The human body's endogenous antioxidant system plays a crucial role in mitigating the adverse effects of oxidative stress.
- Understanding the mechanisms by which antioxidants counteract PM2.5-induced lung injury is vital for developing effective interventions.
Purpose of the Study:
- To investigate the protective role of enhanced endogenous antioxidant capacity against PM2.5-induced pulmonary injury.
- To evaluate a novel mouse model (LiasH/H) with elevated antioxidant levels in response to PM2.5 exposure.
- To elucidate the molecular pathways involved in antioxidant defense against PM2.5 toxicity.
Main Methods:
- A novel mouse model (LiasH/H) with ~150% higher endogenous antioxidant capacity than wild-type (Lias+/+) mice was utilized.
- Mice were exposed to PM2.5 suspension or saline via intratracheal instillation for 7 consecutive days.
- Lung pathology, metal content, and biomarkers of oxidative stress and inflammation were assessed.
Main Results:
- PM2.5 exposure induced significant oxidative stress and inflammation in the lungs of mice.
- LiasH/H mice exhibited significantly increased antioxidant levels and attenuated inflammatory responses compared to wild-type mice following PM2.5 exposure.
- The antioxidant effects in LiasH/H mice were mediated by the activation of the ROS-p38MAPK-Nrf2 pathway.
Conclusions:
- Enhanced endogenous antioxidant capacity, as demonstrated in the LiasH/H mouse model, effectively alleviates PM2.5-induced pulmonary injury.
- The ROS-p38MAPK-Nrf2 pathway is a key mechanism through which Lias enhances antioxidant defense against PM2.5 toxicity.
- This novel mouse model provides a valuable tool for studying the mechanisms of PM2.5-induced lung damage and the role of antioxidants.
