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为探讨年龄相关性黄斑变性的免疫炎症反应机制,采用real-time PCR及ELISA检测β-淀粉样蛋白1-40(Aβ_((1-40)))刺激RPE细胞后IL-33 mRNA及蛋白水平表达,并采用ELISA检测IL-33刺激RPE细胞后炎症因子表达情况及调控产生炎症因子的信号通路。结果发现,Aβ_((1-40))刺激人视网膜色素上皮细胞后能够诱导IL-33因子转录及蛋白水平表达上调,且在人视网膜色素上皮细胞中,IL-33因子分别通过p38 MAPK、ERK1/2信号通路调控促炎症因子IL-6、IL-8的表达。据此说明,IL-33通过调控人视网膜色素上皮细胞产生促炎症因子IL-6、IL-8参与年龄相关性黄斑变性的发生发展。
To investigate the mechanism of immune-inflammation in age-related macular degeneration, the mRNA and protein levels of IL-33 after RPE cells were stimulated by β-amyloid 1-40 (Aβ_ (1-40)) were detected by real-time PCR and ELISA The expression of inflammatory cytokines in IL-33-stimulated RPE cells and the signal pathways regulating the production of inflammatory cytokines were detected by ELISA. The results showed that Aβ_ (1-40) stimulated IL-33 gene transcription and protein expression after stimulated by human retinal pigment epithelial cells. In human retinal pigment epithelium cells, IL-33 was activated by p38 MAPK and ERK1 / 2 signaling regulates the expression of proinflammatory cytokines IL-6 and IL-8. Thus, IL-33 is involved in the development of age-related macular degeneration by regulating the production of proinflammatory cytokines IL-6 and IL-8 in human retinal pigment epithelial cells.