Abstract
The neuroprotective and antioxidative effects of germinated brown rice (GBR), brown rice (BR) and commercially available γ-aminobutyric acid (GABA) against cell death induced by hydrogen peroxide (H2O2) in human neuroblastoma SH-SY5Y cells have been investigated. Results show that GBR suppressed H2O2-mediated cytotoxicity and induced G0/G1 phase cell cycle arrest in SH-SY5Y cells. Moreover, GBR reduced mitochondrial membrane potential (MMP) and prevented phosphatidylserine (PS) translocation in SH-SY5Y cells, key features of apoptosis, and subsequent cell death. GBR exhibited better neuroprotective and antioxidative activities as compared to BR and GABA. These results indicate that GBR possesses high antioxidative activities and suppressed cell death in SH-SY5Y cells by blocking the cell cycle re-entry and apoptotic mechanisms. Therefore, GBR could be developed as a value added functional food to prevent neurodegenerative diseases caused by oxidative stress and apoptosis.
Highlights
Oxidative stress is implicated in the neuronal damage associated with Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotropic lateral sclerosis and cerebral ischemic stroke.The damage is thought to be mediated by reactive oxygen species (ROS) including hydrogen peroxide (H2O2)
Pre-treatment with 1 or 10 μg/mL of GABA, germinated brown rice (GBR) and brown rice (BR) significantly increased the viability of SH-SY5Y cells against H2O2-induced cytotoxicity (Figure 1C)
H2O2 has the ability to induce cell cytotoxicity [20] and results of the current study demonstrated that the physiological concentration of 1 and 10 μg/mL of GABA, GBR and BR were able to counteract the deleterious effect of 250 μM H2O2 (Figure 1C)
Summary
Oxidative stress is implicated in the neuronal damage associated with Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotropic lateral sclerosis and cerebral ischemic stroke. The human neuroblastoma SH-SY5Y cell line is widely used as a model cell system for studying oxidative stress-induced neuronal cell death. It is shown that feeding on GBR diet decreased the accumulation of lead and improved learning and memory deficits in developing rats after Pb exposure that may be due to the antioxidative effects of phenolic compounds and high content of GABA [15]. Studies on the direct effects of GBR on H2O2-induced cytotoxicity and apoptosis are limited, and since neurodegeneration due to oxidative stress is believed to underlie the neurodegenerative diseases, it may be hypothesized that GBR, BR and GABA have some neuroprotective effects. The present study was aimed to examine the neuroprotective and antioxidative effects of GBR in comparison to BR and GABA against H2O2 in RA-differentiated SH-SY5Y neuronal-like cells
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