PDF(Pubmed)
Abstract：
OBJECTIVE: Rhegmatogenous retinal detachment is a severe vision-threatening complication that can result into proliferative vitreoretinopathy (PVR) and re-detachment of the retina if recovery from surgery fails. Inflammation and changes in retinal pigment epithelial (RPE) cells are important contributors to the disease. Here, we studied the effects of simvastatin and amfenac on ARPE-19 cells under inflammatory conditions.
METHODS: ARPE-19 cells were pre-treated with simvastatin and/or amfenac for 24 h after which interleukin (IL)-1α or IL-1β was added for another 24 h. After treatments, lactate dehydrogenase release, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) processing, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activity, prostaglandin E2 (PGE2) level, and extracellular levels of IL-6, IL-8, monocytic chemoattractant protein (MCP-1), vascular endothelial growth factor (VEGF), and pigment epithelium-derived factor, as well as the production of reactive oxygen species (ROS) were determined.
RESULTS: Pre-treatment of human ARPE-19 cells with simvastatin reduced the production of IL-6, IL-8, and MCP-1 cytokines, PGE2 levels, as well as NF-κB activity upon inflammation, whereas amfenac reduced IL-8 and MCP-1 release but increased ROS production. Together, simvastatin and amfenac reduced the release of IL-6, IL-8, and MCP-1 cytokines as well as NF-κB activity but increased the VEGF release upon inflammation in ARPE-19 cells.
CONCLUSIONS: Our present study supports the anti-inflammatory capacity of simvastatin as pre-treatment against inflammation in human RPE cells, and the addition of amfenac complements the effect. The early modulation of local conditions in the retina can prevent inflammation induced PVR formation and subsequent retinal re-detachment.
METHODS: ARPE-19 cells were pre-treated with simvastatin and/or amfenac for 24 h after which interleukin (IL)-1α or IL-1β was added for another 24 h. After treatments, lactate dehydrogenase release, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) processing, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activity, prostaglandin E2 (PGE2) level, and extracellular levels of IL-6, IL-8, monocytic chemoattractant protein (MCP-1), vascular endothelial growth factor (VEGF), and pigment epithelium-derived factor, as well as the production of reactive oxygen species (ROS) were determined.
RESULTS: Pre-treatment of human ARPE-19 cells with simvastatin reduced the production of IL-6, IL-8, and MCP-1 cytokines, PGE2 levels, as well as NF-κB activity upon inflammation, whereas amfenac reduced IL-8 and MCP-1 release but increased ROS production. Together, simvastatin and amfenac reduced the release of IL-6, IL-8, and MCP-1 cytokines as well as NF-κB activity but increased the VEGF release upon inflammation in ARPE-19 cells.
CONCLUSIONS: Our present study supports the anti-inflammatory capacity of simvastatin as pre-treatment against inflammation in human RPE cells, and the addition of amfenac complements the effect. The early modulation of local conditions in the retina can prevent inflammation induced PVR formation and subsequent retinal re-detachment.
摘要：
目的：风源性视网膜脱离是一种严重的视力威胁并发症，如果手术恢复失败，可导致增生性玻璃体视网膜病变（PVR）和视网膜再脱离。视网膜色素上皮（RPE）细胞的炎症和变化是该疾病的重要原因。这里,我们研究了辛伐他汀和氨芬酸在炎症条件下对ARPE-19细胞的影响.
方法：ARPE-19细胞用辛伐他汀和/或氨芬酸预处理24小时，然后再加入白介素（IL）-1α或IL-1β24小时。处理后，乳酸脱氢酶释放，3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑溴化（MTT）处理，核因子κ-活化B细胞（NF-κB）活性的轻链增强剂，前列腺素E2（PGE2）水平，和细胞外水平的IL-6，IL-8，单核细胞趋化蛋白（MCP-1），血管内皮生长因子（VEGF），和色素上皮衍生因子，以及确定了活性氧（ROS）的产生。
结果：用辛伐他汀预处理人ARPE-19细胞可减少IL-6、IL-8和MCP-1细胞因子的产生，PGE2水平，以及炎症时的NF-κB活性，而氨芬酸减少了IL-8和MCP-1的释放，但增加了ROS的产生。一起,辛伐他汀和氨芬酸减少了IL-6，IL-8和MCP-1细胞因子的释放以及NF-κB活性，但增加了ARPE-19细胞炎症时的VEGF释放。
结论：我们目前的研究支持辛伐他汀作为人RPE细胞炎症预处理的抗炎能力，和添加氨芬酸补充效果。视网膜局部条件的早期调节可以防止炎症诱导的PVR形成和随后的视网膜再脱离。
方法：ARPE-19细胞用辛伐他汀和/或氨芬酸预处理24小时，然后再加入白介素（IL）-1α或IL-1β24小时。处理后，乳酸脱氢酶释放，3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑溴化（MTT）处理，核因子κ-活化B细胞（NF-κB）活性的轻链增强剂，前列腺素E2（PGE2）水平，和细胞外水平的IL-6，IL-8，单核细胞趋化蛋白（MCP-1），血管内皮生长因子（VEGF），和色素上皮衍生因子，以及确定了活性氧（ROS）的产生。
结果：用辛伐他汀预处理人ARPE-19细胞可减少IL-6、IL-8和MCP-1细胞因子的产生，PGE2水平，以及炎症时的NF-κB活性，而氨芬酸减少了IL-8和MCP-1的释放，但增加了ROS的产生。一起,辛伐他汀和氨芬酸减少了IL-6，IL-8和MCP-1细胞因子的释放以及NF-κB活性，但增加了ARPE-19细胞炎症时的VEGF释放。
结论：我们目前的研究支持辛伐他汀作为人RPE细胞炎症预处理的抗炎能力，和添加氨芬酸补充效果。视网膜局部条件的早期调节可以防止炎症诱导的PVR形成和随后的视网膜再脱离。
