Acetyl-L-carnitine protects neuronal cells: Roles in vitro and in vivo experiments.

摘要

Accumulation of oxidative damage to mitochondria is considered as a cause of neuronal apoptosis, and leads to Alzheimer's disease. Acetyl-L-carnitine (Alcar), a cellular energy substrate, is known to attenuate oxidative stress. Mechanism of Alcar in reducing oxidative stress and protecting neurons was investigated. Neuroblastoma (SH-SY5Y) and murine cortical neurons were employed. Alcar protected cells from oxidative damage by maintaining mitochondrial polarization, not as antioxidant. Alcar also attenuated reactive oxygen species, tau-hyperphosphorylation and apoptosis. Because Alcar demonstrated positive ameliorating effects in cultured cells, in vivo experiments were consequently performed in young and old mice by adding Alcar in drinking water. The hippocampus of old mice was high in lipid peroxidation when fed an oxidative-stress inducing diet. Feeding Alcar combined with oxidative-stress inducing diet attenuated lipid peroxidation. However, in both age groups, feeding Alcar alone also elevated lipid peroxidation. These results suggest that in vivo Alcar metabolism in tissues or organs may be more complex than cells in culture.