摘要
目的:研究腺嘌呤核苷酸转位酶1(ANT1)在亚硒酸钠抑制脑胶质瘤生长中的作用机制。方法:将不同浓度的亚硒酸钠(0.5、1.0、2.0、4.0μmol/L)侵染人脑胶质瘤细胞SHG44,MTT比色法检测亚硒酸钠对SHG44的增殖的影响;PCR法检测ANT1的表达;提取细胞线粒体后通过观察线粒体的荧光强度,检测SHG44的线粒体膜电位和膜通道开放程度。结果:亚硒酸钠对人脑胶质瘤细胞具有明显的抑制作用,2.0及4.0μmol/L染硒组差异均有统计学意义(P<0.05),ANT1的表达在各染硒组均出现显著性增加(P<0.05);线粒体膜电位在2.0及4.0μmol/L染硒组显著降低(P<0.05),线粒体膜通道转运孔开放程度在1.0、2.0及4.0μmol/L组显著增高(P<0.05)。结论:亚硒酸钠能抑制人脑胶质瘤细胞SHG44地生长,并伴随线粒体膜电位降低和线粒体膜通道转运孔开放程度增加,ANT1可能参与了其作用机制。
Objective： To study the mechanism of adenine nucleotide translocator 1 in the inhibition of sodium selenite to human glioma SHG44 cell. Methods： SHG44 cells were treated with different concentrations of sodium selenite（0.5,1.0,2.0 and 4. 0 μmol/L）. Growth inhibition of SHG44 cells was detected by MTY assay. Expression of ANT1 was detected by PCR method. Mitochondrial permea- bility transition and mitochondrial membrane potential were observed by fluorescence intensity after mi- tochondria was extracted. Results： Sodium selenite suppressed the growth of SHG44 cells significant- ly, and statistical significance was found in 2.0 and 4.0μmol/L groups （P 〈0.05 ）. Expression of ANT1 significantly increased in each selenium group （ P 〈 0.05 ）. Mitoehondrial membrane potential decreased significantly in 2.0 and 4.0μmol/L groups （ P 〈 0.05 ）. Opening degree of mitochondrial permeability transition increased significantly in 1.0, 2.0 and 4.0 μmol/L groups （ P 〈 0.05 ）. Con- clusion： Sodium selenite can suppress the SHG44 cell growth, and ANT1 may be involved in this mechanism, with decreasing mitoehondrial membrane potential and increasing mitochondrial permeabil- ity transition opening degree.
出处
《贵阳医学院学报》
CAS
2012年第6期635-638,共4页
Journal of Guiyang Medical College
基金
武警医学院科研基金面上项目(WYM201118)
武警医学院科研基金博士启动金项目(WYB201110)
