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Abstract Objective： To investigate the effect of UCP2 during the oxidative stress injury procedure of PM2.5 on the rat myocardial cells H9C2. Method： Rat cardiomyocytes H9C2 cell lines were cultured，and divided into 3 groups，the NC group was used of conventional medium stimulus，the PM2.5 group was used of PM2.5 medium stimulus and the PM2.5+siRNA group was used of PM2.5+siRNA medium stimulus. After 48 hours，the activity of reactive oxygen species （ROS） and superoxide dismutase（ SOD）， and the content of malonaldehyde（ MDA） and glutathione（ GSH），were determinated by colorimetric detection.Result：The PM2.5 group of intracellular ROS，MDA， the content of GSH，and the activity of SOD，were respectively（ 69.2±6.3）U/Well，（68.33±1.96）nmol/mgprot，（533.05±10.83）mg/ gprot，（50.37±1.98）U/mgprot.Compared with PM2.5 group，the PM2.5+siRNA group of intracellular ROS was （90.2±6.2）U/Well increased greatly，MDA was（88.44±1.27）nmol/mgprot increased greatly，the content of GSH was（ 421.17±16.90）mg/gprot and the activity of SOD was（30.09±2.02）U/mgprot. Compared the three groups，all the differences were statistically significant（P<0.05）. Conclusion：PM2.5 can lead to myocardial cell damage by oxidative stress， and the silence of UCP2 by RNAi lead to aggravate the injury of H9C2 cells， indicating that UCP2 may play an protective effect during the oxidative stress injury procedure of H9C2 caused by PM2.5.
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