Abstract: Objective Death of retinal ganglion cells(RGCs) during acute glaucoma leads to progressive degeneration of retinal nerves and irreversible blindness. Puerarin has been shown to have antioxidant and anti-neuroinflammatory properties that protect the retina from acute glaucoma. However,the mechanism behind this process remains unclear. Methods In this study,rat model of acute glaucoma was established,and rats were randomly divided into five groups:normal control group, SnPP group, I/ R group, puerarin ( 100 μmol / L ) group and puerarin + SnPP group. Hematoxylin and eosin staining were used to evaluate the retinal conditions in the I/ R group, puerarin group and puerarin + SnPP group. Levels of TNF-α and IL-1β were detected by ELISA and qRT-PCR. Expression levels of cleaved caspase-8,Nrf2,and HO-1 were detected by Western blotting. The expression levels of Brn-3a, β3-tubulin and RBPMS were detected by immunofluorescence. Cell apoptosis and intracellular reactive oxygen species were detected by flow cytometry. Results Puerarin treatment significantly reduced retinal damage and RGC death in acute glaucoma rats,and significantly reduced the production of reactive oxygen species and inflammatory cytokines in the retina. In addition,the reduction of ROS production by puerarin had re-balanced the intracellular redox status,thus contributing to the survival of RGCs in vitro. Puerarin treatment also reduced the production of inflammatory cytokines in vitro. Puerarin inhibited the cell apoptosis and the production of inflammatory cytokine in RGCs through regulation of Nrf2 / HO-1 pathway. Moreover, the neuroprotective effect of puerarin on acute glaucoma was eliminated when SnPP,an HO-1 inhibitor,was administered. Conclusion Our findings identify the underlying mechanism of RGC apoptosis and the neuroprotective effect of a novel therapeutic agent puerarin on acute glaucoma.

Key words: puerarin, Nrf2 / HO-1 pathway, glaucoma, retinal injury