The neuroprotective effects of tocotrienol rich fraction and alpha tocopherol against glutamate injury in astrocytes

Thilaga Rati Selvaraju; Huzwah Khaza’ai; Sharmili Vidyadaran; Mohd Sokhini Abd Mutalib; Ramachandran Vasudevan

doi:10.17305/bjbms.2014.91

Authors

Thilaga Rati Selvaraju Biochemistry Unit, Department of Biomedical Science, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, 43400 Selangor, Malaysia
Huzwah Khaza’ai Biochemistry Unit, Department of Biomedical Science, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, 43400 Selangor, Malaysia
Sharmili Vidyadaran Department of Immunology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, 43400 Selangor, Malaysia
Mohd Sokhini Abd Mutalib Department of Nutrition and Dietetic, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, 43400 Selangor, Malaysia
Ramachandran Vasudevan Institute of Gerontology, Universiti Putra Malaysia, Serdang, 43400 Selangor, Malaysia

DOI:

https://doi.org/10.17305/bjbms.2014.91

Keywords:

Vitamin E, tocotrienol rich fraction, alpha tocopherol, glutamate, astrocytes

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.