Ji Yinghong, Cai Lei, Zheng Tianyu, Ye Hongfei, Rong Xianfang, Rao Jun, Lu Yi
Department of Ophthalmology, Eye & ENT Hospital of Fudan University, No. 83 Fenyang Road, Shanghai, 200031, China.
Mol Cell Biochem. 2015 Mar;401(1-2):87-95. doi: 10.1007/s11010-014-2294-x. Epub 2014 Dec 2.
Cataract is the most common eye disease that causes blindness in patients. Ultraviolet B (UVB) irradiation is considered an important factor leading to cataract by inducing apoptosis in human lens epithelial cells (HLECs), but the mechanism is currently unclear. In this study, we investigated HLECs under different intensities of UVB irradiation and different exposure time. The annexin V-FITC/propidium iodide staining results showed that UVB irradiation could efficiently lead to HLECs apoptosis in time- and dose-dependent manner. The expression of pro-apoptotic Bax gene was promoted by UVB irradiation, while anti-apoptotic Bcl-2 gene expression was inhibited at both transcript and protein levels. Notably, the ratio of Bax/Bcl-2 displayed a high and positive correlation to the proportion of apoptotic HLECs. Mitochondrial dysfunction was also observed with rapid loss of potential (∆Ψ m), as well as changes of the levels of reactive oxygen species, malondialdehyde, total antioxidative capabilities, and superoxide dismutase. In caspase pathway, the level of caspase-3 protein increased after UVB irradiation. All these discovered changes may play important roles in UVB-induced HLECs apoptosis, and would be helpful in understanding the mechanism of UVB-induced cataract and providing potential prevention and treatment strategies.
白内障是导致患者失明的最常见眼病。紫外线B（UVB）照射被认为是通过诱导人晶状体上皮细胞（HLECs）凋亡而导致白内障的一个重要因素，但目前其机制尚不清楚。在本研究中，我们对不同强度UVB照射及不同暴露时间下的HLECs进行了研究。膜联蛋白V-异硫氰酸荧光素/碘化丙啶染色结果表明，UVB照射能够以时间和剂量依赖性方式有效导致HLECs凋亡。UVB照射促进促凋亡Bax基因的表达，而抗凋亡Bcl-2基因在转录和蛋白水平均受到抑制。值得注意的是，Bax/Bcl-2比值与凋亡HLECs的比例呈高度正相关。还观察到线粒体功能障碍，表现为膜电位（∆Ψm）迅速丧失，以及活性氧、丙二醛、总抗氧化能力和超氧化物歧化酶水平的变化。在半胱天冬酶途径中，UVB照射后半胱天冬酶-3蛋白水平升高。所有这些发现的变化可能在UVB诱导的HLECs凋亡中起重要作用，有助于理解UVB诱导白内障的机制并提供潜在的预防和治疗策略。
