ABSTRACT Glaucoma is a progressive optic neuropathy and improper treatment may cause irreversible damage to visual function. Gastrodin is an effective active substance extracted from Gastrodia elata and possesses antioxidant… Click to show full abstract
ABSTRACT Glaucoma is a progressive optic neuropathy and improper treatment may cause irreversible damage to visual function. Gastrodin is an effective active substance extracted from Gastrodia elata and possesses antioxidant as well as anti-inflammatory properties. However, the therapeutic potential of gastrodin for retinal ischemia/reperfusion (I/R) injury remains unclear. We adopted oxygen and glucose deprivation/reoxygenation (OGD/R) to induce R28 cells with the aim of simulating glaucomatous neurodegeneration. CCK-8 analysis and TUNEL were applied for examining cell proliferation and apoptosis . In addition, RT-qPCR and ELISA were performed to test the releases of inflammatory factors in cells . Related indicators of intracellular oxidative stress and ROS production were detected by corresponding kits. Moreover, western blot was applied to assay the expressions of PI3K/AKT/Nrf2 pathway-related proteins. OGD/R induction contributed to the decreased cell viability and reduced Bcl-2 protein expression, while the protein contents of Bax, Cyto-C, c-caspase 9 and c-PARP as well as ROS production were ascended. The co-treatment of hypoxia and gastrodin greatly improved R28 cell viability but effectively suppressed cell apoptosis, ROS level and the releases of OGD/R-induced inflammatory factors as well as oxidative stress. In addition, OGD/R stimulation reduced Nrf2, accompanied by a decrease in the phosphorylation levels of PI3K and AKT. Gastrodin significantly promoted the activation of PI3K/AKT/Nrf2 signaling pathway in R28 cells, which was then counteracted by PI3K/AKT inhibitors. In conclusion, the present study suggested that gastrodin has a protective effect on OGD/R-induced R28 cell injury, which is achieved through the activation of the PI3K/AKT/Nrf2 signaling pathway. Graphical abstract
               
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