Abstract
Background: Oxidative stress plays a role in diabetic retinopathy. L-Carnitine is an endogenous mitochondrial membrane compound.
Objective: To elucidate the protective effects of L-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 (??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 L-carnitine.
Results:L-Carnitine (12 h) inhibited high glucose-mediated cell loss and restored mitochondrial function including a reversion of ??m loss and cytochrome c release. Cell apoptosis triggered by high glucose was also inhibited by L-carnitine, characterized by the downregulation of caspase-9, caspase-3 and Bax/Bcl-2. Furthermore, L-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:L-Carnitine may protect RGCs from high glucose-induced injury through the inhibition of oxidative damage, mitochondrial dysfunction and, ultimately, cell apoptosis.
Objective: To elucidate the protective effects of L-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 (??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 L-carnitine.
Results:L-Carnitine (12 h) inhibited high glucose-mediated cell loss and restored mitochondrial function including a reversion of ??m loss and cytochrome c release. Cell apoptosis triggered by high glucose was also inhibited by L-carnitine, characterized by the downregulation of caspase-9, caspase-3 and Bax/Bcl-2. Furthermore, L-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:L-Carnitine may protect RGCs from high glucose-induced injury through the inhibition of oxidative damage, mitochondrial dysfunction and, ultimately, cell apoptosis.
| Original language | English |
|---|---|
| Pages (from-to) | 123-130 |
| Number of pages | 8 |
| Journal | Pharmacology |
| Volume | 94 |
| Issue number | 3-4 |
| DOIs | |
| Publication status | Published - Nov 2014 |
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