Background: The major event in the development of diabetes-related blindness and vision impairment is the onset of retinal cell damage. Overall awareness of insulin-like growth factor-2 (IGF2) mechanisms emphasizes its protective behavior in retinal cells that help to provide new information about the development of treatment for retinal complications. Objectives: This study analyzes the effect of in vitro changes associated with the cell survival and rescue mechanism in IGF2 inhibition and activation using chromeceptin and IGF2 peptides in ARPE-19 cells cultured in high glucose conditions. Method: Cell death was induced using high glucose (15 mmol/L), IGF2 inhibition was done using chromeceptin (1 µM) (Sigma Aldrich, Saint Louis, MO, USA), and IGF2 activation was done using IGF2 peptide (10 ng/mL). The cells were analyzed for changes in cell proliferation, apoptosis markers, antioxidant molecules, and alteration of cytokines. Results: The study demonstrated that cells lacking IGF2 exhibited a significant increase in reactive oxygen levels with apoptosis patterns. Also, gene expression analysis by qRT-PCR demonstrated a significant increase in Yes-associated protein 1, CDK2, TNF-α, and BIRC5 genes in cells under high glucose stress and IGF inhibition compared to control. Further, the cytokine analysis also revealed that cells devoid of IGF2 activated an increase in cytokines such as IL-8, CX43, ICAM-1, IL-17, CCL3, and MCP-1 and decreased paraoxonase compared to normal control cells. On the other hand, ARPE-19 cells grown in high glucose shows that IGF2 increases the survival genes with reduced levels of inflammatory cytokines. Conclusion: The finding of the investigation, therefore, shows that the use of IGF2 activators may prevent the progression of ocular dysfunction in the control of diabetes-related complications.
Neuroimmunomodulation

中文翻译：

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胰岛素样生长因子 2 的激活减轻视网膜细胞损伤并在糖尿病视网膜病变体外模型中发挥保护作用

背景：糖尿病相关失明和视力障碍发展的主要事件是视网膜细胞损伤的发生。对胰岛素样生长因子 2 (IGF2) 机制的整体认识强调其在视网膜细胞中的保护行为，这有助于提供有关视网膜并发症治疗发展的新信息。目的：本研究在高糖条件下培养的 ARPE-19 细胞中分析了与细胞存活和拯救机制相关的体外变化对 IGF2 抑制和激活的影响。方法：使用高葡萄糖 (15 mmol/L) 诱导细胞死亡，使用 chromeceptin (1 µM) (Sigma Aldrich, Saint Louis, MO, USA) 进行 IGF2 抑制，使用 IGF2 肽 (10 ng/mL) 进行 IGF2 激活. 分析细胞的细胞增殖、凋亡标志物、抗氧化分子和细胞因子改变的变化。结果：该研究表明，缺乏 IGF2 的细胞表现出具有凋亡模式的活性氧水平显着增加。此外，通过 qRT-PCR 进行的基因表达分析表明，与对照相比，在高葡萄糖应激和 IGF 抑制下的细胞中 Yes 相关蛋白 1、CDK2、TNF-α 和 BIRC5 基因显着增加。此外，细胞因子分析还显示，与正常对照细胞相比，缺乏 IGF2 的细胞激活了细胞因子的增加，例如 IL-8、CX43、ICAM-1、IL-17、CCL3 和 MCP-1，并降低了对氧磷酶。另一方面，在高糖条件下生长的 ARPE-19 细胞表明 IGF2 增加了存活基因，同时炎症细胞因子水平降低。结论：因此，调查结果表明，在控制糖尿病相关并发症的过程中，使用 IGF2 激活剂可以预防眼功能障碍的进展。
神经免疫调节