Abstract
Tocotrienol rich fraction (TRF) is an extract of palm oil, which consists of 25% alpha tocopherol (α-TCP) and 75% tocotrienols. TRF has been shown to possess potent antioxidant, anti-inflammatory, anticancer, neuroprotection, and cholesterol lowering activities. Glutamate is the main excitatory amino acid neurotransmitter in the central nervous system of mammalian, which can be excitotoxic, and it has been suggested to play a key role in neurodegenerative disorders like Parkinson's and Alzheimer's diseases. In this present study, the effects of vitamin E (TRF and α-TCP) in protecting astrocytes against glutamate injury were elucidated. Astrocytes induced with 180 mM of glutamate lead to significant cell death. However, glutamate mediated cytotoxicity was diminished via pre and post supplementation of TRF and α-TCP. Hence, vitamin E acted as a potent antioxidant agent in recovering mitochondrial injury due to elevated oxidative stress, and enhanced better survivability upon glutamate toxicity.
Highlights
The expansion of an in vitro model for the early stages of neurodegenerative disease is a current inevitability
The microvolume of tetrazolium test (MTT) assay is a potential indicator of the viability of cells, as it was used to evaluate the activity of enzyme within the mitochondria, which can reduce the yellow MTT solution to purple formazan [26]
The effects of Tocotrienol rich fraction (TRF) and α-TCP upon glutamate induced cytotoxicity were evaluated via MTT cell viability assay
Summary
The expansion of an in vitro model for the early stages of neurodegenerative disease is a current inevitability. Neurodegenerative disease is one of the leading causes of death throughout the world [1]. It has been considered as one of the major problems for our aging society and well-defined as a group of illnesses of the nervous system, which comprises of brain, spinal cord, as well as peripheral nerves [1]. Oxidative stress and reactive oxygen species (ROS) have been implicated in the development of neurodegenerative diseases [3]. An in vitro model of these processes would improve our understanding of the development of neurodegenerative diseases, and enhance the development of further treatments
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