中文摘要：

采用C57BL6小鼠作为模型,SO2（7 mg·m^-3）动式吸入染毒28 d,每天染毒6 h;SO2吸入染毒开始后的第1-5 d,每天在SO2吸入染毒结束后对小鼠进行腹腔注射Ba P（40 mg·kg^-1（b.w.））,1 d注射1次.吸入染毒结束后,采用荧光定量PCR技术检测小鼠心肌细胞中由核DNA（n DNA）编码的细胞色素C氧化酶亚基CO4和由线粒体DNA（mt DNA）编码的ATP合酶亚基ATP6,以及调控线粒体呼吸链组分的核转录因子PGC1-α、NRF1和mt TFA的mRNA水平;并采用Western blot技术检测上述3种线粒体调控基因的蛋白表达.结果发现,SO2和Ba P复合暴露后,小鼠心肌线粒体氧化磷酸化复合体亚基CO4和ATP6的mRNA表达水平均显著降低,调控基因PGC1-α、NRF1和mt TFA的mRNA和蛋白水平也显著降低.提示小鼠在SO2和Ba P复合暴露后,可能通过降低心肌中NRF1表达,影响其对mt TFA的调控,进一步抑制相关基因组的转录和翻译,最终可能导致小鼠心肌线粒体的氧化磷酸化功能受损,进而引发心血管疾病.

英文摘要：

C57BL6 male mice were exposed to SO2（ 7 mg·m^-3） for 28 days,6 hours per day. In the first 5 days of SO2 inhalation,mice were injected intraperitoneally with Ba P（ 40 mg·kg^-1（ b. w.）） once a day,which was dissolved in oil. The mRNA levels of two mitochondrial oxidative phosphorylation related genes（ CO4,ATP6） and three mitochondrial transcript factors（ PGC1-α,NRF1,mt TFA） were analyzed by real-time RT-PCR after 28 days＇ SO2 inhalation. And the protein levels of the above three mitochondrial transcript factors were detected by Western blot. The results demonstrated that the co- exposure of SO2 and Ba P statistically elevated the mRNA expression of CO4 and ATP6,combined with decreased mRNA and protein levels of mitochondrial transcript factors and mt TFA. It is indicated that conjunction of SO2 and Ba P induced mouse myocardial cell mitochondria damage might related to NRF1 expression,which then inhibited the transcription and translation of TFAM and mitochondrial oxidative phosphorylation related genes. And the myocardial cell mitochondria damage might result in cardiovascular diseases.