Obestatin prevents H2O2-induced damage through activation of TrkB in RGC-5 cells

Abstract

Backgroud: In the early stage of diabetic retinopathy, the damage of retinal ganglion cells already exists, promoting the development of the disease. The aim of this study was to investigate the protective role and the mechanisms of obestatin against H₂O₂-induced damage in RGC-5 cells.

Methods: RGC-5 cells were incubated with various concentrations of obestatin for 24h before H₂O₂ added. The survival rates of RGC-5 were measured by MTT assay. The expression of apoptosis-related proteins and TrkB pathway-related proteins were detected by Western blot analysis.

Results: Our data showed that H₂O₂ evidently decreased the survival rate of RGC-5 cells. However, obestatin pretreatment reversed the decreased activity. Moreover, obestatin effectively increased the expression of Bcl-2 and decreased the expression of Bax. In addition, obestatin potentially plays a role in protecting RGC-5 by activating of TrkB. Obestatin notablely increased the phosphorylation of TrkB, AKT and ERK1/2. All these effects of obestatin can be inhibited by GLP-1R antagonist exendin (9-39).

Conclusions: Obestatin prevents H₂O₂-induced damage in RGC-5 cells by activating TrkB pathway. Moreover, GLP-1R is closely related to the function of obestatin in RGC-5 cells.

Keywords: Diabetic retinopathy; Obestatin; Oxidative stress; Retinal ganglion cells; TrkB.