Metformin Protects ARPE-19 Cells from Glyoxal-Induced Oxidative Stress

Oxidative Medicine and Cellular Longevity
Sichang QuJingfa Zhang

Abstract

The protective effects and mechanisms of metformin against oxidative stress were evaluated both in vivo and in vitro. ARPE-19 cells comprised the normal group, the glyoxal-treated group (0.5 mM glyoxal), and the glyoxal+metformin group (0.5 mM glyoxal and 0.1 mM metformin). In the in vitro model, differences in cell viability, ROS production, NO products, cellular apoptosis, and the expressions of phospho-AMPKα, total-AMPKα, Sirt1, Nrf2, TXNIP, ZO-1, and Occludin were assessed. In the glyoxal-treated group, cell viability and NO production were decreased, while ROS production and cell apoptosis were increased (p < 0.05), compared with the control group. These changes were prevented by metformin treatment. Protein expressions of phospho-AMPKα, Sirt1, TXNIP, ZO-1, and Occludin, but not Nrf2, were decreased significantly in the glyoxal-treated group compared to normal controls. Metformin treatment significantly increased the above protein expressions and slightly increased TXNIP expression. Immunofluorescence showed that metformin prevented the glyoxal-induced, disorganized tight junctions in ARPE-19 cells. To confirm metformin's protection, Sprague-Dawley rats were injected intravenously with sodium iodate (SI) to induce oxidativ...Continue Reading

Methods Mentioned

BETA
dissection
Assay
Protein Assay

Related Concepts

Related Feeds

Autophagy & Aging: Inhibitors

The feed focuses on the role of nuclear export inhibitors and their effect on autophagy and the aging process.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis