半乳糖凝集素-3 抑制物可改善 ARPE-19 细胞高糖诱导的氧化应激和炎症反应。
Inhibition of galectin-3 ameliorates high-glucose-induced oxidative stress and inflammation in ARPE-19 cells.
机构信息
Department of Endocrinology, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
Department of Ophthalmology, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
出版信息
Cutan Ocul Toxicol. 2022 Jun;41(2):179-186. doi: 10.1080/15569527.2022.2081701. Epub 2022 Jun 5.
PURPOSE
Retinal pigment epithelium (RPE) has been found to be participated in the pathogenesis of DR in recent years. Galectin-3 (Gal-3) is involved in many diabetic complications and ophthalmological diseases. However, the role of Gal-3 in RPE cells in DR remains unknown. This study aims to investigate the role of Gal-3 in ARPE-19 cells under high glucose treatment.
MATERIALS AND METHODS
ARPE-19 cells were cultured under normal or high glucose (HG) for 48 h. Expression of Gal-3 was inhibited by Si-Gal-3 transfection. Apoptosis was checked by flow cytometry. Oxidative stress was checked by measuring ROS, MDA levels, and SOD activities. Occludin and ZO-1 expression were checked by immunofluorescence staining. Genes involved in inflammatory response were measured by real-time PCR and Western blot.
RESULTS
Gal-3 expression could be increased by HG treatment in ARPE-19 cells. Gal-3 knockdown might reduce oxidative stress, apoptosis, and gene expression of VCAM-1, ICAM-1, and integrin-β1 induced by HG treatment. The gene expression of IL-1β could be markedly promoted by HG treatment and this increasement was partly alleviated by Gal-3 knockdown only at the mRNA level. The reduced expression of ZO-1 and occludin caused by HG could also be improved by Gal-3 knockdown.
CONCLUSION
Gal-3 participated in increased oxidative stress and inflammatory response caused by HG in ARPE-19 cells.
目的
近年来发现视网膜色素上皮（RPE）参与了 DR 的发病机制。半乳糖凝集素-3（Gal-3）参与了许多糖尿病并发症和眼科疾病。然而，Gal-3 在 DR 中 RPE 细胞中的作用尚不清楚。本研究旨在探讨 Gal-3 在高糖处理的 ARPE-19 细胞中的作用。
材料和方法
将 ARPE-19 细胞在正常或高糖（HG）下培养 48 小时。通过 Si-Gal-3 转染抑制 Gal-3 的表达。通过流式细胞术检查细胞凋亡。通过测量 ROS、MDA 水平和 SOD 活性来检查氧化应激。通过免疫荧光染色检查 occludin 和 ZO-1 的表达。通过实时 PCR 和 Western blot 测量参与炎症反应的基因。
结果
HG 处理可增加 ARPE-19 细胞中的 Gal-3 表达。Gal-3 敲低可能会降低 HG 处理诱导的氧化应激、细胞凋亡以及 VCAM-1、ICAM-1 和整合素-β1 的基因表达。HG 处理可显著促进 IL-1β 的基因表达，而 Gal-3 敲低仅在 mRNA 水平部分缓解这种增加。HG 引起的 ZO-1 和 occludin 表达减少也可以通过 Gal-3 敲低得到改善。
结论
Gal-3 参与了 HG 引起的 ARPE-19 细胞中氧化应激和炎症反应的增加。
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