Chudhary Maryam, Zhang Chenghong, Song Shiyu, Ren Xiang, Kong Li
Department of Histology and Embryology, College of Basic Medicine, Dalian Medical University, Dalian, Liaoning 116044, P.R. China.
Teaching Laboratory of Morphology, College of Basic Medicine, Dalian Medical University, Dalian, Liaoning 116044, P.R. China.
Exp Ther Med. 2021 Jun;21(6):576. doi: 10.3892/etm.2021.10008. Epub 2021 Mar 31.
Intense exposure to artificial bright light increases the risk of retinal damage resulting in blurred vision and blindness. Long-term exposure to bright light elevates oxidative stress-induced apoptosis, which results in photoreceptor cell degeneration. However, to the best of our knowledge, the molecular mechanism associated with light-induced retinopathy remains unclear. In the present study, the mechanisms involved in light-induced oxidative stress and apoptosis were investigated along with the protective effects of (EGb 761) in photoreceptor cell degeneration. EGb 761 was administered to mice at a dose of 50 or 100 mg/kg for 7 days prior to exposure to bright light (5,000 lux for 24 h). Furthermore, photoreceptor cell disorders were evaluated using electroretinogram (ERG) and H&E staining analyses. The expression levels of antioxidant genes and proteins ERK, thioredoxin (Trx) and nuclear factor erythroid 2-related factor 2 (Nrf-2) and the induction of apoptosis cytochrome c (Cyc), cleaved caspase-3 and Bax, were determined by reverse transcription-quantitative PCR and western blotting. ERG and histological analysis revealed that exposure to bright light induced functional and morphological changes to the photoreceptor cells. Exposure to bright light increased the levels of Cyc, cleaved caspase-3 and Bax, and decreased the levels of phosphorylated (p-) Erk, Nrf-2 and thioredoxin (Trx). However, treatment of mice with EGb 761 increased the expression levels of antiapoptotic (Bcl-2) and antioxidant (p-Erk, Trx and Nrf-2) proteins and decreased the expression levels of the apoptotic genes (Cyc, cleaved caspase-3 and Bax). Based on these findings, the present study suggested that prolonged exposure to light induces photoreceptor cell degeneration, where EGb 761 treatment may serve a therapeutic effect on the development of photoreceptor cell degeneration.
强烈暴露于人工强光会增加视网膜损伤的风险，导致视力模糊和失明。长期暴露于强光会加剧氧化应激诱导的细胞凋亡，从而导致光感受器细胞变性。然而，据我们所知，与光诱导性视网膜病变相关的分子机制仍不清楚。在本研究中，我们研究了光诱导氧化应激和细胞凋亡的机制，以及银杏叶提取物（EGb 761）对光感受器细胞变性的保护作用。在暴露于强光（5000勒克斯，持续24小时）之前，以50或100毫克/千克的剂量给小鼠施用EGb 761，持续7天。此外，使用视网膜电图（ERG）和苏木精-伊红（H&E）染色分析评估光感受器细胞紊乱情况。通过逆转录定量PCR和蛋白质印迹法测定抗氧化基因和蛋白质ERK、硫氧还蛋白（Trx）和核因子红细胞2相关因子2（Nrf-2）的表达水平，以及凋亡细胞色素c（Cyc）、裂解的半胱天冬酶-3和Bax的诱导情况。ERG和组织学分析表明，暴露于强光会导致光感受器细胞发生功能和形态变化。暴露于强光会增加Cyc、裂解的半胱天冬酶-3和Bax的水平，并降低磷酸化（p-）Erk、Nrf-2和硫氧还蛋白（Trx）的水平。然而，用EGb 761处理小鼠会增加抗凋亡（Bcl-2）和抗氧化（p-Erk、Trx和Nrf-2）蛋白的表达水平，并降低凋亡基因（Cyc、裂解的半胱天冬酶-3和Bax）的表达水平。基于这些发现，本研究表明，长时间暴露于光会诱导光感受器细胞变性，而EGb 761治疗可能对光感受器细胞变性的发展具有治疗作用。
