Pachymic Acid Alleviates Oxidative Damage of Retinal Cells Induced by Sodium Iodate or Hydrogen Peroxide by Activating the Nrf2/HO-1 Signaling Pathway

Abstract

Background: Pachymic acid (PA), extracted from the traditional Chinese medicinal herb Poria cocos ( P cocos) is reported to protect organs such as the liver and lungs from damage. This study investigated the effect of PA on oxidative stress in the retina in vivo and in vitro. Methods: In vitro, retinal pigment epithelial (RPE) cells were treated with hydrogen peroxide to establish a cell model of oxidative damage. The viability of ARPE-19 cells was measured using an MTT kit. Apoptosis of the cells was detected using flow cytometry, and the expression of Caspase-3, Bax, and Bcl-2 was determined. The oxidative stress level was evaluated by observing the production of superoxide dismutase, catalase, and GSH-Px using ELISA in mice serum. The retinal oxidative damage model was induced by intravenous injection of sodium iodate (SI) into the tail vein of mice. OCT, HE, and TUNEL staining monitored the structure and the apoptosis of the mouse retina. The regulatory oxidative factors nuclear transcription factor E2-related factor 2 (Nrf2) and HO-1 were determined using fluorescence staining. Results: H2O2 decreased the viability of RPE cells, which was recovered after PA administration and was shown to reduce the cell apoptosis rate, the expression of Bax, caspase-3, and the production of ROS. In vivo, the thinning of the retina and the apoptosis rate in the retinal tissue of mice caused by the administration of SI were reversed by treatment with PA. Furthermore, PA administration caused the translocation of Nrf2 and increased the expression of HO-1, and the application of these inhibitors inhibited this effect. Conclusion: PA protects RPE cells from oxidative stress and apoptosis by activating the Nrf2/HO-1 pathway, and it prevents retinal damage by halting the progression of retinal thinning in a mouse model of retinal oxidative damage.