摘要
目的研究阿霉素对乳鼠心肌细胞损伤的机制。方法将原代培养的乳鼠心肌细胞分成两组:对照组和阿霉素处理组,通过流式细胞术检测心肌细胞内氧化应激水平,采用MTT比色法检测细胞活性,应用Real Time-PCR技术检测Gclc、SLC7A11的表达水平,通过紫外分光光度法检测细胞内谷胱甘肽浓度。结果阿霉素升高乳鼠心肌细胞内氧化应激水平,对乳鼠心肌有损伤作用。经阿霉素处理后,乳鼠心肌细胞内Gclc、SLC7A11的表达水平及谷光氨肽浓度显著降低。结论阿霉素通过下调乳鼠心肌细胞Gclc、SLC7A11表达水平,降低细胞内谷光氨肽浓度,升高细胞内氧化应激水平造成乳鼠心肌细胞损伤。
Objective To investigate the injury mechanism of doxorubicin to neonatal cardio- myocytes. Methods Primary cultured neonatal cardiomyocytes were divided into 2 groups： control and Doxo groups. The reactive oxygen species （ROS） level was detected by flow cyto- metry, cell viability was detected by MTF assay, and mRNA expression of Gclc, SLC7All were detected by real time PCR in each group. Results Doxorubicn increased ROS level, and produced injury in neonatal cardiomyoeytes. The mRNA expression of Gclc, SLC7All and concentration of GSH decreased in neonatal cardiomyocytes. Conclusion Doxorubien pro- duced injury in neonatal cardiomyocytes through decreasing the mRNA expression of Gclc, SLC7All, dereasing GSH concentration, increasing ROS level.
出处
《哈尔滨医科大学学报》
CAS
北大核心
2013年第1期35-37,42,共4页
Journal of Harbin Medical University
基金
2010年黑龙江省教育厅科学技术研究面上项目(11551280)
