Tanshinone II-A protects retinal ganglion cells against retinal ischemia/reperfusion injury

We aimed to evaluate the protective effects of tanshinone II-A (TanIIA) on retinal ischemia and reperfusion (I/R) injury. The primary retinal ganglion cells (RGCs) were isolated from the retinae of Sprague-Dawley (SD) rats and then were induced retinal I/R injury in vitro. The RGCs subjected to I/R injury were treated with different concentrations of TanIIA (1.0 mM, 2.5 mM or 5.0 mM, respectively). Cell viability, Caspase-3 activity, LDH release, cell apoptosis and the level of mitochondria-derived ROS of different treatment groups were analyzed, respectively. Additionally, the expression levels of key molecules involving in Akt/MAPK signaling pathway, such as Akt, p-Akt, mTOR, p-mTOR, MAPK and p-MAPK, and apoptotic proteins, like Bcl2 and Bax, were determined by western blot. TanIIA treatment promoted cell viability and decreased caspase-3 activity and LDH release in a dose-dependent manner. What's more, TanIIA treatment inhibited cell apoptosis and the production of mitochondria-derived ROS in a dose-dependent manner. Besides, TanIIA treatment resulted in a markedly decrease in the expression of key proteins involving in Akt/MAPK signaling pathway, such as Akt, p-Akt, mTOR, p-mTOR, MAPK and p-MAPK, as well as the expression of apoptotic protein Bax. Our findings indicate that TanIIA treatment may promote cell viability and inhibit cell apoptosis after cells were induced retinal I/R injury. Moreover, TanIIA may protect RGCs against retinal I/R injury via inhibiting cell apoptosis or suppressing Akt/MAPK signaling pathway. TanIIA may serve as a potential therapeutic reagent for the treatment of ocular diseases.