Objective:To investigate the impact of the air pollutant benzo[a]pyrene(BaP)on myocardial ischemia-reperfusion(IR)injury and further explore the pivotal role of the Aryl Hydrocarbon Receptor(Ahr)in this process.Methods:C57BL/6J mice were administered BaP via inhalation(15mg/kg),followed by the construction of a myocardial ischemia-reperfusion injury model.The extent of myocardial damage in the experimental group and control group was assessed through Evans Blue/TTC staining,TUNEL staining,echocardiography,and Masson's trichrome staining.Additionally,RT-PCR and immunofluorescence co-localization were employed to investigate the potential mechanisms mediated by Ahr.Results:Compared to the control group,mice in the experimental group exhibited more severe myocardial damage.RT-PCR results indicated that,following BaP exposure,there was a significant increase in the mRNA expression levels of Ahr downstream target genes and inflammation-related genes.Immunofluorescence staining demonstrated prominent expression of Ahr on cardiac macrophages.Conclusions:These findings suggest that the air pollutant BaP exacerbates myocardial ischemia-reperfusion injury by activating Ahr,which in turn promotes the secretion of inflammatory factors by macrophages.
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