低硒与心肌细胞氧化损伤机制及凋亡相关基因的表达

目的观察低硒对大鼠心肌组织脂质过氧化物、心肌细胞超微结构及细胞凋亡相关基因的影响。方法建立对照组、低硒组、补硒组3个组别大鼠模型，结合光镜及电镜下心肌组织及其超微结构病理变化，对其血清硒、谷胱甘肽过氧化物酶（GPx）、心肌组织匀浆丙二醛（MDA）水平及心肌细胞凋亡相关基因Bcl-2、Bax、P53蛋白表达进行检测及对比分析。结果低硒组大鼠血清硒水平及血清GPx活性水平均显著低于正常对照组和低硒加硒组，低硒组大鼠心肌组织匀浆MDA水平显著高于正常对照组和低硒加硒组。低硒组大鼠心肌线粒体膜及细胞核膜上清晰可见高电子密度反应产物聚集。低硒组大鼠心肌Bcl-2、Bax、P53的基因表达（PI％）均显著高于正常对照组大鼠；低硒组大鼠Bcl-2基因表达（PI％）显著低于低硒加硒组大鼠；而Bax、P53的基因表达（PI％）均显著高于低硒加硒组。结论低硒可以引起线粒体膜、细胞核膜磷脂过氧化损伤，进而造成心肌细胞线粒体损伤，同时可引起大鼠心肌细胞抑制凋亡基因Bcl-2和促进凋亡基因Bax、P53的基因表达相应增强，但BcF2／Bax比值相对下降，促进凋亡的发生。补硒可以诱导抑制凋亡基因Bcl-2基因表达的上调，使其基因表达增强，同时相对抑制促凋亡基因Bax和P53的表达。

The relationship between low-selenium and the mechanisms of oxygenated lesion of myocardial cells and the expression of apoptosis-related genes

Objective To study the effects of low selenium on myocardial tissue lipid peroxidation, myocardial ultrastructure and apoptosis related genes. Methods Male Sprague-Dawley rats were randomly divided into three groups and had been fed with low-selenium diet of Keshan disease area, selenium-supplementing diet and control diet of Xi＇an area respectively for 15 weeks. Serum level of selenium and serum GPx activity were measured. The con- tent of MDA in myocardial homogenate supernatant of rats and Apoptoic genetic expression （including Bcl-2, Bax and P53） were also detected and analyzed. Result Serum level of selenium （μg/ml） and Serum GPx activity （U） in low-selenium group were significantly lower than that in selenium-supplementing group and the control group. The content of MDA （nmol/mg） of myocardial homogenate supernatant of low-selenium group was significantly higher than that in the other two groups. Rat heart mitochondria membrane and nuclear membrane are clearly visible accu- mulation of high electron density reaction products. In low-selenium group the number of Bcl-2, Bax and P53 posi- tive expression was significantly higher than that in the control group. Also Bax and P53 positive expression was sig- nificantly higher than that in Se-supplementing group except for Bcl-2. Conclusion Low selenium can cause mito- chondrial membrane and nuclear membrane phospholipid peroxidation, and further induce mitochondrial damage. Meanwhile it can cause inhibition of myocardial cell apoptosis gene Bcl-2 and promote apoptosis gene Bax, P53 gene expression in the corresponding increase. However, it causes the relative decline in Bcl-2/Bax ratio, and promotes apoptosis. Se supplement can induce inhibition of apoptosis gene Bcl-2 gene expression up to enhance gene expression, and can also cause the relative inhibition of pro-apoptotic gene Bax and P53 expression.