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Anti‐ inflammatory effects of thymoquinone in LPS‐ stimulated BV‐2 murine microglia cells (730.2)
Author(s) -
Taka Equar,
Mazzio Elizabeth,
Goodman Carl,
Reeams Renee,
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.730.2
Subject(s) - thymoquinone , microglia , chemokine , lipopolysaccharide , inflammation , pharmacology , neuroprotection , cytokine , immunology , chemistry , medicine , biochemistry , antioxidant
Thymoquinone (TQ) is one the main pharmacologically active constituents of the black cumin seeds (Nigella sativa) believed to be responsible for therapeutic effects on chronic inflammatory conditions such as arthritis and asthma. In this study, we investigate the possible neuroprotective action of TQ in activated microglia cells. We hypothesized that the anti‐inflammatory properties of TQ are mediated in part by inhibiting the formation of pro‐inflammatory cytokines, chemokine’s and other inflammatory mediators. In this study, we evaluated the anti‐inflammatory activity of TQ in lipopolysaccharide (LPS) (1µg/ml) stimulated microglia cells in the presence or absence of TQ (10µM). Cytokines/chemokine's were profiled using a RayBio antibody protein array and NO release was evaluated using the Griess reagent assay. In addition, cytokine antibody array results were validated using PCR array and ELISA. Our results showed that TQ significantly inhibited Pro‐inflammatory cytokines including IL‐6, IL‐1β, IL‐12p40/70, Growth Colony Stimulating Factor (G‐CSF), and pro‐inflammatory chemokine’s such as MCP‐5, IP‐10, MCP‐1 and inflammatory mediators NO production in LPS stimulated BV‐2 cells. In conclusion, the results obtained suggest that TQ could have a neuroprotction potential and may provide a mean for the treatment of neuro‐inflammation that occurs in neurodegenerative diseases such as Alzheimer and Parkinson’s diseases. Grant Funding Source : Supported by NIH grants NIMHD G12 MD007582 and P20 MD006738