Background Optic nerve injury is a severe complication of traumatic brain injury, which may lead to permanent and potentially loss of vision. Arbutin (ARB) is a natural hydroquinone glycoside, has been widely utilized to treat pigmented disorders. However, the role of ARB in optic nerve injury is still unclear. The study attempted to explore the effect of ARB on H2O2-induced oxidative injury in RGCs. Methods RGCs were treated with different concentrations of H2O2 to construct a cell oxidative injury model. Subsequently, the effects of ARB on these injured cells were examined through testing cell viability, apoptosis and their associated factors. MicroRNA-29a (miR-29a) inhibitor was transfected into RGCs, and the regulatory effect of miR-29a inhibition on H2O2-injured cells was detected. Further, the important signaling pathways of MEK/ERK and p38MAPK were determined to uncover the underlying mechanism. Results We firstly used H2O2 to induce RGCs injury, and subsequent experiments found that ARB significantly alleviated H2O2-induced cell injury in RGCs by promoting cell viability, reducing apoptosis, and regulating the protein levels of cell growth-associated factors. Increasing expression of miR-29a was observed in ARB and H2O2 treated cells. Moreover, miR-29a inhibition significantly abrogated the protective effect of ARB on H2O2-injured RGCs. NRAS was predicated as a direct target gene of miR-29a. Mechanistically, ARB blocked MEK/ERK and p38MAPK pathways by up-regulating miR-29a. Conclusions These data demonstrated that ARB protected RGCs against oxidative injury induced by H2O2 through blocking MEK/ERK and p38MAPK signaling pathways by up-regulation of miR-29a.
