Hubei Key Laboratory of Bioinorganic Chemistry & Materia Medica, School of Chemistry and Chemical Engineering, Huazhong University of Science and Technology, 1037 Luoyu Road, Hongshan, Wuhan 430074, China.
Int J Mol Sci. 2016 Feb 10;17(2):231. doi: 10.3390/ijms17020231.
Selenium is an essential micronutrient for humans. Much of selenium's beneficial influence on health is attributed to its presence within 25 selenoproteins. Selenoprotein R (SelR), known as methionine sulfoxide reductase B1 (MsrB1), is a selenium-dependent enzyme that, like other Msrs, is required for lens cell viability. In order to investigate the roles of SelR in protecting human lens epithelial (hLE) cells against damage, the influences of SelR gene knockdown on d-galactose-induced apoptosis in hLE cells were studied. The results showed that both d-galactose and SelR gene knockdown by siRNA independently induced oxidative stress. When SelR-gene-silenced hLE cells were exposed to d-galactose, glucose-regulated protein 78 (GRP78) protein level was further increased, mitochondrial membrane potential was significantly decreased and accompanied by a release of mitochondrial cytochrome c. At the same time, the apoptosis cells percentage and the caspase-3 activity were visibly elevated in hLE cells. These results suggested that SelR might protect hLE cell mitochondria and mitigating apoptosis in hLE cells against oxidative stress and endoplasmic reticulum (ER) stress induced by d-galactose, implying that selenium as a micronutrient may play important roles in hLE cells.
硒是人体必需的微量元素。硒对健康的有益影响很大程度上归因于其存在于 25 种硒蛋白中。硒蛋白 R（SelR），也称为蛋氨酸亚砜还原酶 B1（MsrB1），是一种依赖硒的酶，与其他 Msrs 一样，是晶状体细胞活力所必需的。为了研究 SelR 在保护人晶状体上皮（hLE）细胞免受损伤中的作用，研究了 SelR 基因敲低对 hLE 细胞中 d-半乳糖诱导的细胞凋亡的影响。结果表明，d-半乳糖和 SelR 基因通过 siRNA 敲低均可独立诱导氧化应激。当 SelR 基因沉默的 hLE 细胞暴露于 d-半乳糖时，葡萄糖调节蛋白 78（GRP78）蛋白水平进一步增加，线粒体膜电位显著降低，并伴有线粒体细胞色素 c 的释放。同时，hLE 细胞中的凋亡细胞百分比和 caspase-3 活性明显升高。这些结果表明，SelR 可能保护 hLE 细胞的线粒体，并减轻由 d-半乳糖诱导的氧化应激和内质网（ER）应激对 hLE 细胞的凋亡，这意味着硒作为一种必需微量元素可能在 hLE 细胞中发挥重要作用。
