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Abstract #82313 Published in IGR 20-4
The Neuroprotective Effect of the Adiponectin Receptor Agonist AdipoRon on Glutamate-Induced Cell Death in Rat Primary Retinal Ganglion Cells
Uchida T; Ueta T; Honjo M; Aihara MJournal of Ocular Pharmacology and Therapeutics 2019; 35: 535-541
To determine whether the adiponectin receptor (AdipoR) agonist AdipoRon inhibits glutamate-induced neuronal cell death and to investigate the neuroprotective mechanism of AdipoRon in rat primary retinal ganglion cells (RGCs). The expression pattern of AdipoR1 and AdipoR2 in rat retina and primary RGCs was examined by immunostaining. The neuroprotective effect of AdipoRon on glutamate-induced cell death was evaluated in rat primary RGCs. Cellular levels of reactive oxygen species (ROS) were also measured. Peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), estrogen-related receptor-α (Esrra), mitochondrial transcription factor A (TFAM), peroxisome proliferator-activated receptor α (PPARα), and catalase mRNA levels were examined. The expression of AdipoR1 and AdipoR2 was confirmed in rat retina and primary RGCs. AdipoRon significantly increased the survival rate of glutamate-induced cell death and decreased ROS production. Additionally, the mRNA levels of PGC-1α, Esrra, and TFAM were upregulated by AdipoRon. These results suggest that AdipoRon has a neuroprotective effect by inhibiting ROS production via upregulation of PGC-1α, Esrra, and TFAM against glutamate-induced RGC death.
Full article
Classification:
5.1 Rodent (Part of: 5 Experimental glaucoma; animal models)
11.8 Neuroprotection (Part of: 11 Medical treatment)
11.14 Investigational drugs; pharmacological experiments (Part of: 11 Medical treatment)
