Cyanin Chloride Inhibits Hyperbaric Pressure-Induced Decrease of Intracellular Glutamate-Aspartate Transporter in Rat Retinal Müller Cells

Abstract EN

Purpose.

Glaucoma is the leading cause of irreversible blindness throughout the world.

The pathogenesis of glaucoma is complex, and neuroprotection is a crucial aspect of therapy.

High concentrations of extracellular glutamate are toxic to the optic nerve.

The glutamate-aspartate transporter (GLAST) in retinal Müller cells is involved in the development of glaucoma.

Anthocyanin has been reported to protect retinal neurons.

We hypothesize that cyanin chloride, a type of anthocyanin, can inhibit hyperbaric pressure-induced GLAST decreases in cultured rat retinal Müller cells and may serve as a potential neuroprotective agent in glaucoma treatment.

Materials and Methods.

Sprague Dawley rat Müller cells were cultured in a hyperbaric pressure device at 60 mmHg additional pressure and treated with cyanin chloride (10 μmol/L, 30 μmol/L, or 50 μmol/L) or vehicle for 2 hours.

Cell survival rates (SRs) were evaluated by an MTT assay.

GLAST mRNA and protein expression were determined by western blot and RT-PCR analyses, respectively.

Results.

Cell SR was significantly decreased in the 60 mmHg additional hyperbaric pressure group compared to the control group (P<0.01).

Cyanin chloride treatment significantly improved SR under 60 mmHg additional pressure (P<0.01).

GLAST mRNA and protein expression levels in Müller cells were significantly reduced in the 60 mmHg hyperbaric pressure group compared to the control group (P<0.01), but cyanin chloride significantly inhibited hyperbaric pressure-induced decreases in GLAST expression (P<0.01).

Conclusion.

Our results support our hypothesis and demonstrate that cyanin chloride can protect rat retinal Müller cells from hyperbaric pressure-induced decreases of GLAST.