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The antioxidant effects of thymoquinone in lipopolysaccharide‐activated BV2 murine microglia cells (89.5)
Author(s) -
Duval Makini,
Taka Equar,
Mazzio Elizabeth,
Soliman Karam
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.89.5
Subject(s) - microglia , thymoquinone , chemistry , neuroinflammation , antioxidant , oxidative stress , neun , microbiology and biotechnology , lipopolysaccharide , inflammation , pharmacology , biochemistry , immunology , biology , immunohistochemistry
Activation of microglia, resident immune cells in the central nervous system (CNS), is implicated in the pathogenesis and progression of neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease. They may cause a vicious self‐perpetuating neuronal degeneration cycle via excessive release of superoxide radicals in the system. We explored the effects of thymoquinone (TQ), the main active constituent of Nigella sativa seed oil, as an antioxidant agent in microglial activation. We hypothesized that the antioxidant properties of TQ are mediated in part by reducing proteins involved in oxidative stress induced by microglia activation. In this study, BV2 cells were stimulated with LPS in the presence or absence of TQ. To profile the effect of TQ on global protein expression of BV2 microglial cells, two‐dimensional (2D)‐gel electrophoresis with MALDI‐TOF/TOF (matrix‐assisted laser desorption/ionization ‐ time of flight) analysis was employed. Additionally, the effect of TQ on microglia activation was evaluated using immunocytochemistry‐ immunofluorescence (ICC‐IF). The results obtained indicate that TQ decreased the expression of 60 kDa heat shock, fatty acid binding, and CD68 [ED1] proteins in LPS stimulated BV2 cells. These findings suggest that the intervention of microglial activation process could be a promising therapeutic target in the treatment of a number of neurodegenerative conditions. Grant Funding Source : Supported by NIH grants: NIMHD G12 MD007582 and P20 MD006738