天津医药 ›› 2021, Vol. 49 ›› Issue (2): 131-135.doi: 10.11958/20202452

• 细胞与分子生物学 • 上一篇    下一篇

叶黄素通过SIRT1/NLRP3信号通路提高人视网膜色素上皮细胞存活率的机制研究 #br#

,马利方   

  1. 1北京同仁医院体检科(邮编100730);2北京大学第三医院生殖医学中心

  • 收稿日期:2020-09-02 修回日期:2020-10-30 出版日期:2021-02-15 发布日期:2021-02-02
  • 通讯作者: 马利方 E-mail:21511633@qq.com
  • 基金资助:
    NLRP1炎症小体调控多囊卵巢综合征患者卵巢颗粒细胞炎症反应和代谢紊乱的作用机制研究

Study on the mechanism of improving the activity of human retinal pigment epithelial cells by lutein through the SIRT1/NLRP3 signaling pathway #br#

  • Received:2020-09-02 Revised:2020-10-30 Published:2021-02-15 Online:2021-02-02
  • Contact: Li-Fang Ma E-mail:21511633@qq.com

摘要: 目的 探讨叶黄素对高浓度葡萄糖诱导后人视网膜色素上皮细胞(ARPE-19细胞)内过氧化应激反应、炎 症反应与细胞增殖活性的改善作用及调控机制。方法 使用不同浓度的叶黄素和高浓度葡萄糖同时处理ARPE-19 细胞后,应用 CCK-8 检测细胞增殖活性变化,应用酶联免疫吸附试验检测炎性细胞因子水平变化,应用 CMH 2DCFDA探针法检测活性氧(ROS)水平变化,应用荧光定量PCR检测SIRT1与NLRP3 mRNA表达水平变化。结果 在高葡萄糖环境下,ARPE-19细胞内炎性细胞因子白细胞介素(IL)-1β、IL-6、IL-18、肿瘤坏死因子(TNF)-α和ROS 的表达水平显著高于对照组(P<0.05),细胞存活率低于对照组(P<0.01)。与葡萄糖组比较,叶黄素组SIRT1 mRNA 表达水平和细胞存活率显著上调,而 NLRP3 mRNA 表达水平显著下调(P<0.05)。结论 叶黄素可通过 SIRT1/ NLRP3信号通路改善人视网膜色素上皮细胞内的过氧化应激反应与炎症反应,进而提高细胞存活率。

关键词: 叶黄素, 视网膜色素上皮, 糖尿病视网膜病变, NLR家族, 热蛋白结构域包含蛋白3, 炎症, 细胞因子类, 氧化性应激, SIRT1/NLRP3信号通路

Abstract: Objective  To investigate the improvement effect and mechanism of lutein on roxidative stress,
inflammation and cell activity in human retinal pigment epithelial cells (ARPE-19 cells) induced by high concentration of
glucose.
Methods After treatment of ARPE-19 cells with different concentrations of lutein solution and high concentration
of glucose, CCK-8 was used to detect changes in cell viability. Enzyme-linked immunosorbent assay was used to detect
changes in inflammatory cytokine levels. The CM-H
2DCFDA probe method was used to detect the changes in reactive
oxygen species (ROS) levels. The changes in the expression levels of
SIRT1 and NLRP3 were detected by real-time
quantitative PCR.
Results In the environment of high glucose, the expression levels of interleukin (IL)-1β, IL-6 and tumor
necrosis factor (TNF)-α in ARPE-19 cells were significantly increased, ROS levels were significantly increased, and cell
viability was significantly decreased than those of control group (
P0.05). After treating ARPE-19 cells with lutein, the
expression level of
SIRT1 was significantly up-regulated (P0.05), and the expression level of NLRP3 mRNA was
significantly down-regulated (
P0.05). Conclusion Lutein can improve oxidative stress and inflammatory response in
human retinal pigment epithelial cells through the SIRT1/NLRP3 signaling pathway, thereby increasing the cell viability.

Key words: lutein, retinal pigment epithelium, diabetic retinopathy, NLR family, pyrin domain-containing 3 protein,
inflammation,
cytokines, oxidative stress, SIRT1/NLRP3 signaling pathway

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