Chlorogenic acid relieved oxidative stress injury in retinal ganglion cells through IncRNA-TUG1/Nrf2

Abstract

Objective: To discover the possible underlying mechanism of Chlorogenic acid (CGA) in protecting against oxidative stress injury in glaucoma. Methods: LncRNA TUG1 and Nrf2 expressions were detected by qRT-PCR and Western blot. Retinal ganglion cell (RGC) viability and apoptosis were measured by MTT and flow cytometry, respectively. Reactive oxygen species (ROS) level was determined by reactive oxygen species assay kit. The interaction between lncRNA TUG1 and Nrf2 was confirmed by RNA pull-down and RIP assay. Results: IPL thickness and lncRNA TUG1 expression were significantly decreased in glaucoma mice model, and CGA treatment increased IPL thickness and lncRNA TUG1 expression. In vitro H2O2-induced RGCs, RGC viability was significantly decreased, and ROS level and cell apoptosis were significantly increased. CGA up-regulated lncRNA TUG1 and Nrf2 expressions, decreased cell apoptosis and ROS production in RGCs, and increased RGCs viability. We further verified the interaction between lncRNA TUG1 and Nrf2, and proved Nrf2 was positively regulated by lncRNA TUG1. We found CGA promoted Nrf2 expression through lncRNA-TUG1, and further verified CGA protected RGCs from oxidative stress through regulating lncRNA TUG1/Nrf2. In vivo experiments showed TUG1 knockdown abrogated therapeutic effect of CGA on glaucoma. Conclusion: CGA increased RGC viability and decreased ROS level and RGC apoptosis after oxidative stress injury through lncRNA TUG1/Nrf2 pathway, which protected against glaucoma.