Ambient air fine particulate matter (PM_2.5) may increase cardiovascular disease risks. In this study, we investigated the miR-208/GATA4/myosin heavy chain (MHC) regulation mechanisms on cardiac injury in rats after PM_2.5 exposure via an animal inhalation device. The results showed that PM_2.5 exposure for 2 months caused pathological heart injury, reduced nucleus-cytoplasm ratio, and increased the levels of CK-MB and cTnI, showing cardiac hypertrophy. Oxidative stress and inflammatory responses were also observed in rats’ hearts exposed to PM_2.5. Of note, PM_2.5 exposure for 2-month significantly elevated GATA4 and β-MHC mRNA and protein expression compared with the corresponding controls, along with the high-expression of miR-208b. The ratios of β-MHC/α-MHC expression induced by PM_2.5 were remarkably raised in comparison to their controls. It suggested that the up-regulation of miR-208b/β-MHC and GATA4 and the conversion from α-MHC to β-MHC may be the important causes of cardiac hypertrophy in rats incurred by PM_2.5.

环境空气细颗粒物 (PM _2.5 ) 可能会增加心血管疾病的风险。在本研究中，我们通过动物吸入装置研究了 miR-208/GATA4/肌球蛋白重链 (MHC) 对大鼠 PM _2.5暴露后心脏损伤的调节机制。结果显示，PM _2.5暴露2个月引起病理性心脏损伤，核质比降低，CK-MB和cTnI水平升高，表现为心脏肥厚。在暴露于 PM _2.5的大鼠心脏中也观察到氧化应激和炎症反应。值得注意的是，与相应对照相比，PM _2.5暴露 2 个月显着升高了 GATA4 和 β-MHC mRNA 和蛋白表达，同时 miR-208b 也高表达。与对照组相比，PM _2.5诱导的β-MHC/α-MHC表达比率显着升高。提示miR-208b/β-MHC和GATA4的上调以及α-MHC向β-MHC的转化可能是PM _2.5引起大鼠心肌肥厚的重要原因。