Ginsenoside Rg1 protects human retinal pigment epithelial ARPE-19 cells from toxicity of high glucose by up-regulation of miR-26a.

AIMS: The therapeutic strategies for diabetic retinopathy (DR) are disappointing. Ginsenoside Rg1 (Rg1) extracted from Panax ginseng can induce glucose uptake and lower oxidative stress. We aimed to explore the effect of Rg1 on DR using human retinal pigment epithelium cells (ARPE-19).

MAIN METHODS: ARPE-19 cells were grown in high glucose (HG) to simulate DR. Cell viability, apoptosis, ROS generation and miR-26a level were examined by CCK-8 assay, flow cytometry assay, DCFH-DA staining and RT-qPCR, respectively. Expression of proteins associated with viability, apoptosis and oxidative stress was measured by Western blot analysis. Effects of Rg1 on HG-induced alteration were assessed. Moreover, whether miR-26a was involved in Rg1-associated modulation was verified. Finally, the involvements of the ERK and Wnt/β-catenin pathways were analyzed by Western blot analysis.

KEY FINDINGS: HG reduced cell viability while promoted apoptosis and oxidative stress in ARPE-19 cells. Rg1 ameliorated HG-induced cell injury. The expression of miR-26a was up-regulated by Rg1 in HG-treated cells, and miR-26a inhibition obviously reversed the effects of Rg1 on HG-treated cells. Finally, we found the ERK and Wnt/β-catenin pathways were inhibited by Rg1 through up-regulation of miR-26a.

SIGNIFICANCE: Rg1 protected ARPE-19 cells against HG-induced injury through up-regulating miR-26a, along with inhibition of the ERK and Wnt/β-catenin pathways. Rg1 might be a potential therapeutic drug for DR.