【摘要】 [目的]观察SO2对大鼠肺细胞凋亡相关基因mRNA和蛋白表达的影响。[方法]运用荧光实时定量RT- PCR和免疫组化技术研究了不同浓度SO2(0、14、28、56 mg/m3)吸入对大鼠肺细胞p53、bax、bcl-2三种细胞凋亡相关基因mRNA和蛋白表达的影响。[结果]肺中p53和bax mRNA表达水平及bax/bcl-2比值呈剂量依赖性增加,在低浓度SO2(14mg/m3)吸入条件下,p53、bax mRNA表达水平及bax/bcl-2比值虽然有升高趋势,但统计学上未见显著差异, 在SO2浓度为28．00和56．00mg/m3时均为显著增加(与对照组相比,p53:在14mg/m3为1．07倍,在28mg/m3为1．23倍, 在56 mg/m3为1．39倍;bax:在14 mg/m3为1．12倍,在28 mg/m3为1．77倍,在56 mg/m3为2．26倍;bax/bcl-2比值:在 14 mg/m3为1．13倍,在28 mg/m3为2．19倍,在56 mg/m3为3．01倍);而bcl-2 mRNA表达水平呈剂量依赖性降低,在低浓度SO2(14mg/m3)吸入条件下,bcl-2 mRNA水平虽然有降低趋势,但统计学上未见显著差异,在SO2浓度为28．00和 56．00mg/m3时显著降低(与对照组相比,bcl-2:在14mg/m3为0．99倍,在28mg/m3为0．78倍,在56mg／m3为0．73倍)。免疫组化的实验结果表明吸入SO2后大鼠肺中p53和bax蛋白表达水平呈剂量依赖性增加,而’bcl-2蛋白表达水平呈剂量依赖性降低。[结论] SO2可以改变凋亡相关基因的表达,表明SO2可诱导大鼠肺细胞凋亡,这可能与一些凋亡相关疾病的发生有关。这些机制的阐明有助于对SO2毒作用机制的理解和所致疾病的治疗。更多还原

【Abstract】 [Objective] In order to study expression of apoptosis-related genes in lungs from rats exposed to SO2. [Methods] The mRNA and protein levels of p3, bax, bcl-2 were analyzed in lungs of rats exposed to different concentrations of SO2(0, 14, 28, 56 mg/m3)using a real-time reverse transcription-polymerase china reaction ( RT-PCR )assay and immunohistochemistry method, respectively. [ Results] The results showed that mRNA levels of p53, bax and ratio of bax/bcl-2 increased in a dose-dependent manner, and at the concentrations of 28 and 56 mg/m3 SO2 their increases were significant (for p53: 1.07-fold at 14 mg/m3, 1.23-fold at 28 mg/m3 and 1.39-fold at 56 mg/m3, for bax: 1.12-fold at 14 mg/m3, 1.77-fold at 28 mg/m3 and 2.26-fold at 56 mg/m3, for ratio of bax/bcl-2: 1.13-fold at 14 mg/m3, 2.19-fold at 28 mg/m3 and 3.01-fold at 56 mg/m3, compared with the control group respectively), while mRNA levels of bcl-2 decreased in a dose-dependent manner, and at the concentration of 28 and 56 mg/m3 SO2 the decrease was significant( 0.99-fold at 14 mg/m3, 0.78-fold at 28 mg/m3 and 0.73-fold at 56 mg/m3 compared with the control group )in lungs of rats exposed to SO2. Dose-dependent increases in p53 and bax protein levels in the lungs were observed after SO2 inhalation, while decrease in bcl-2 protein levels was found using immunohistochemistry method. [ Conclusion ] These results lead to conclusion that SO2 exposure can change the expression of apoptosis-related genes, and it suggests that SO2 can induce apoptosis in lung and this may have relations with some apoptosis-related diseases. Elucidating the expression patterns of those genes due to SO2 inhalation may be critical to our understanding mechanisms of SO2 effects and helpful for the therapeutic intervention.更多还原