Acer okamotoanum protects SH-SY5Y neuronal cells against hydrogen peroxide-induced oxidative stress
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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.
KeywordsAcer okamotoanum Apoptosis Hydrogen peroxide Inflammation Oxidative stress
This work was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2015R1D1A1A01058868), Republic of Korea. This research was supported by Global Ph.D. Fellowship Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2016_H1A2A1906940).
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Conflict of interest
The authors declare no potential conflicts of interests.
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