Acer okamotoanum protects SH-SY5Y neuronal cells against hydrogen peroxide-induced oxidative stress.

Oxidative stress by over-production of reactive oxygen species (ROS) in brain is widely known as a cause of neurodegenerative disease. We investigated protective effects of Acer okamotoanum against oxidative stress by hydrogen peroxide (H2O2) in SH-SY5Y neuronal cells. Acer okamotoanum reduced ROS production and lactate dehydrogenase release in H2O2-induced SH-SY5Y cells, resulting in elevation of cell viability. To elucidate protective mechanisms, we measured inflammation and apoptosis-associated protein expressions. Treatment with A. okamotoanum dose-dependently decreased pro-inflammatory proteins such as inducible nitric oxide synthase and cyclooxygenase-2. Treatment with A. okamotoanum showed down-regulation of pro-apoptosis genes such as cleaved caspase-3, cleaved caspase-9, and Bax, and up-regulation of anti-apoptosis protein including Bcl-2, in H2O2-induced SH-SY5Y cells. We demonstrated potential anti-inflammatory and anti-apoptotic effect of A. okamotoanum in H2O2-induced SH-SY5Y cells. These results suggest that A. okamotoanum may possess neuroprotective potential, but further study is necessary to elucidate its pharmacological effects in neurodegenerative diseases.