Atorvastatin and captopril mitigated PM2.5-induced systolic blood pressure increases, endothelial dysfunction, and vascular reactive oxygen species formation in exposed mice.
Does atorvastatin or captopril mitigate PM2.5-induced cardiovascular and pulmonary damage in a mouse exposure model?
Atorvastatin and captopril mitigate PM2.5-induced cardiovascular damage, including blood pressure increases and endothelial dysfunction, in a mouse model, suggesting potential protective strategies for high-risk patients exposed to air pollution.
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.
Junglas et al. (Thu,) conducted a other in PM2.5-induced cardiovascular damage. Atorvastatin or captopril vs. PM2.5 exposure without treatment was evaluated on Systolic blood pressure increases, endothelial dysfunction, and reactive oxygen species formation. Atorvastatin and captopril mitigated PM2.5-induced systolic blood pressure increases, endothelial dysfunction, and vascular reactive oxygen species formation in exposed mice.