Hubei Key Laboratory of Bioinorganic Chemistry & Materia Medica, School of Chemistry and Chemical Engineering, Huazhong University of Science and Technology, Hubei 430074, PR China; Department of Biochemistry and Molecular Biology, Chongqing Medical University, Chongqing, 400016, PR China.
Life Sci. 2013 Feb 27;92(3):193-201. doi: 10.1016/j.lfs.2012.11.021. Epub 2012 Dec 24.
To determine roles of methionine sulfoxide reductase B1 (MsrB1) in protecting lens mitochondria against oxidative damage, the influences of MsrB1 gene silencing on high-glucose-induced apoptosis in human lens epithelial (HLE) cells were studied.
Our study used four groups of cells: normal control, MsrB1 gene silenced, high glucose (30mM) exposed and MsrB1 gene silenced cells followed with high glucose exposure. In all cases we detected cell viability, cell apoptosis rate, intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) levels, alteration of mitochondrial membrane potential, release of mitochondrial cytochrome c as well as an increase in activity of caspase-3.
The results showed that MsrB1 gene silencing by short interfering RNA (siRNA) in HLE cells clearly resulted in oxidative stress, decrease in mitochondrial membrane potential and release of mitochondrial cytochrome c as well as an increase in activity of caspase-3 and the percentage of apoptotic cells. When MsrB1-silenced HLE cells were exposed to high glucose, characteristic of high-glucose-induced mitochondrial dysfunctions were further exacerbated.
MsrB1 plays important roles in protecting HLE cell mitochondria against oxidative damage and inhibits oxidative stress-induced apoptosis in diabetic cataracts by scavenging ROS.
为了确定甲硫氨酸亚砜还原酶 B1（MsrB1）在保护晶状体线粒体免受氧化损伤中的作用，研究了 MsrB1 基因沉默对人晶状体上皮（HLE）细胞高葡萄糖诱导凋亡的影响。
本研究使用了四组细胞：正常对照组、MsrB1 基因沉默组、高葡萄糖（30mM）暴露组和 MsrB1 基因沉默组后高葡萄糖暴露组。在所有情况下，我们都检测了细胞活力、细胞凋亡率、细胞内活性氧（ROS）和丙二醛（MDA）水平、线粒体膜电位的改变、线粒体细胞色素 c 的释放以及 caspase-3 活性的增加。
结果表明，HLE 细胞中短干扰 RNA（siRNA）对 MsrB1 基因的沉默导致明显的氧化应激，线粒体膜电位降低，线粒体细胞色素 c 释放以及 caspase-3 活性和凋亡细胞百分比增加。当 MsrB1 沉默的 HLE 细胞暴露于高葡萄糖时，高葡萄糖诱导的线粒体功能障碍的特征进一步加剧。
MsrB1 通过清除 ROS 在保护 HLE 细胞线粒体免受氧化损伤和抑制糖尿病性白内障中氧化应激诱导的凋亡方面发挥重要作用。
