Key result
Atorvastatin and captopril mitigate PM2.5-induced blood pressure elevation and vascular oxidative stress.
Why the study?
Particulate matter contributes to air pollution-related health hazards, and cardiovascular disease patients are particularly susceptible to air pollution-mediated heart and vascular damage.
Does atorvastatin or captopril mitigate cardiovascular and pulmonary dysfunction in a mouse model of PM2.5 exposure?
Does atorvastatin or captopril mitigate cardiovascular and pulmonary dysfunction in a mouse model of PM2.5 exposure?
Prophylactic atorvastatin and captopril attenuate PM2.5-induced endothelial dysfunction and vascular oxidative stress in a murine model, providing a mechanistic basis for their protective effects against air pollution.
Does not support clinical use against PM2.5 exposure; hypothesis-generating for human pollution-protection trials.
Particulate matter (PM) is a significant contributor to air pollution-associated negative health effects, and cardiovascular disease patients are more susceptible to air pollution-mediated damage of the heart and vessels. The present study investigated the protective effects against PM-induced cardiovascular damage by classic cardiovascular drugs, as used for the standard therapy of cardiovascular disease patients. Male C57BL/6J mice were exposed to ambient PM2.5 (<2.5 µm) for 3 days with or without treatment with the cholesterol-lowering drug atorvastatin (20 mg/kg/d) or the angiotensin-converting enzyme (ACE) inhibitor captopril (50 mg/kg/d). Both drugs mitigated PM2.5-induced systolic blood pressure increases and partially prevented endothelial dysfunction, as reflected by a mixed effect on endothelial nitric oxide synthase phosphorylation. Both drugs ameliorated reactive oxygen species (ROS) formation and phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX-2) expression in the vasculature of PM2.5-exposed mice. Pulmonary ROS levels showed a minor improvement by the treatments, whereas Nox2 mRNA expression was not diminished. Only captopril showed some anti-inflammatory effects in the heart and lung of PM2.5-exposed mice, whereas both drugs failed to reduce systemic inflammation measured in plasma. These findings offer new insights into potential mitigation strategies for PM2.5-induced cardiovascular complications, particularly for patients at higher cardiovascular risk, like those with coronary artery or ischemic heart disease or hypertension.
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Junglas et al. (2026) studied Particulate matter (PM2.5)-induced cardiovascular damage. Atorvastatin or captopril vs. PM2.5 exposure without treatment and fresh air control was evaluated on Systolic blood pressure, endothelial dysfunction, and reactive oxygen species formation. Both atorvastatin and captopril mitigated PM2.5-induced systolic blood pressure increases, partially prevented endothelial dysfunction, and ameliorated vascular reactive oxygen species formation.
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