Effects of <smlcap>L</smlcap>-Carnitine on High Glucose-Induced Oxidative Stress in Retinal Ganglion Cells

<jats:p>Background: Oxidative stress plays a role in diabetic retinopathy. <smlcap>L</smlcap>-Carnitine is an endogenous mitochondrial membrane compound. Objective: To elucidate the protective effects of <smlcap>L</smlcap>-carnitine on high glucose-induced oxidative stress in retinal ganglion cells (RGCs). Methods: Hoechst 33258 staining was used to estimate cell loss. Mitochondrial function was predicted by mitochondrial membrane potential (&#x0394;&#x03A8;m) measurement. The expression of apoptosis-related protein was measured by Western blotting. Assays for reactive oxygen species (ROS) accumulation, lipid peroxidation, total antioxidative capacity (T-AOC) and antioxidant defense enzymes were completed to explain the antioxidative capacity of <smlcap>L</smlcap>-carnitine. Results:<smlcap>L</smlcap>-Carnitine (12 h) inhibited high glucose-mediated cell loss and restored mitochondrial function including a reversion of &#x0394;&#x03A8;m loss and cytochrome c release. Cell apoptosis triggered by high glucose was also inhibited by <smlcap>L</smlcap>-carnitine, characterized by the downregulation of caspase-9, caspase-3 and Bax/Bcl-2. Furthermore, <smlcap>L</smlcap>-carnitine inhibited high glucose-induced ROS production and lipid peroxidation and promoted endogenous antioxidant defense components including superoxide dismutase, glutathione peroxidase, catalase and T-AOC in a concentration-dependent manner. Conclusions:<smlcap>L</smlcap>-Carnitine may protect RGCs from high glucose-induced injury through the inhibition of oxidative damage, mitochondrial dysfunction and, ultimately, cell apoptosis.</jats:p>