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IL-10 通过调节 VEGF 抑制孔源性视网膜脱离的视网膜色素上皮细胞增殖和迁移。

IL-10 inhibits retinal pigment epithelium cell proliferation and migration through regulation of VEGF in rhegmatogenous retinal detachment.

机构信息

Department of Ophthalmology, The Affiliated Hospital of Yan'an University, Yan'an, Shaanxi 716000, P.R. China.

Department of Ophthalmology, The Second Affiliated Hospital of Xi'an Medical University, Xi'an, Shaanxi 710004, P.R. China.

出版信息

Mol Med Rep. 2018 May;17(5):7301-7306. doi: 10.3892/mmr.2018.8787. Epub 2018 Mar 20.

DOI:10.3892/mmr.2018.8787
PMID:29568872
Abstract

Rhegmatogenous retinal detachment (RRD) is a disorder of the eye that affects physical and mental health. Retinal pigment epithelium (RPE) is closely associated with RRD, and it is hypothesized that RPE-secreted inflammatory cytokines may induce early pathological changes of RRD and may participate in RPE proliferation and migration. The present study determined a role for interleukin (IL)‑10 as an RPE‑secreted immune regulatory factor that contributes to RRD. A rat RRD model was established and RPE cells were isolated and cultivated. RPE cells were randomly divided into four groups, three treated with different concentrations of IL‑10 (100, 50, and 20 mM) and one untreated. RPE cell proliferation was evaluated by MTT assay and the activity of caspase‑3 was also measured. RPE cell invasion was determined by Transwell assay. Vascular endothelial growth factor A (VEGF) expression was examined by reverse transcription‑quantitative polymerase chain reaction and western blotting; IL‑1 and IL‑6 levels were measured by ELISA. IL‑10 treatment suppressed RPE cell proliferation and migration, promoted caspase‑3 activity, inhibited VEGF mRNA and protein expression, and downregulated the secretion of inflammatory cytokines IL‑1 and IL‑6 in RRD group compared with the untreated Model group. The aforementioned effects of IL‑10 became more evident with increasing IL‑10 concentration. IL‑10 suppressed inflammation, facilitated RPE cell apoptosis and inhibited cell proliferation and migration through the regulation of VEGF expression.

摘要

孔源性视网膜脱离(RRD)是一种影响身心健康的眼部疾病。视网膜色素上皮(RPE)与 RRD 密切相关,据推测,RPE 分泌的炎症细胞因子可能引发 RRD 的早期病理变化,并可能参与 RPE 的增殖和迁移。本研究确定白细胞介素(IL)-10 作为 RPE 分泌的免疫调节因子在 RRD 中的作用。建立大鼠 RRD 模型并分离和培养 RPE 细胞。将 RPE 细胞随机分为四组,分别用不同浓度的 IL-10(100、50 和 20 mM)处理三组和一组未处理。通过 MTT 法评估 RPE 细胞增殖,同时还测量了 caspase-3 的活性。通过 Transwell 测定法检测 RPE 细胞侵袭。通过逆转录-定量聚合酶链反应和蛋白质印迹法检测血管内皮生长因子 A(VEGF)的表达;通过 ELISA 测定 IL-1 和 IL-6 的水平。与未处理的模型组相比,IL-10 处理抑制了 RPE 细胞的增殖和迁移,促进了 caspase-3 的活性,抑制了 VEGF mRNA 和蛋白表达,并下调了 RRD 组中炎症细胞因子 IL-1 和 IL-6 的分泌。随着 IL-10 浓度的增加,IL-10 的上述作用变得更加明显。IL-10 通过调节 VEGF 的表达抑制炎症,促进 RPE 细胞凋亡,并抑制细胞增殖和迁移。

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