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Inhibition of neuroinflammation by thymoquinone requires activation of Nrf2/ARE signalling.

Abstract：

:Thymoquinone is an antioxidant phytochemical that has been shown to inhibit neuroinflammation. However, little is known about the potential roles of intracellular antioxidant signalling pathways in its anti-inflammatory activity. The objective of this study was to elucidate the roles played by activation of the Nrf2/ARE antioxidant mechanisms in the anti-inflammatory activity of this compound. Thymoquinone inhibited lipopolysaccharide (LPS)-induced neuroinflammation through interference with NF-κB signalling in BV2 microglia. Thymoquinone also activated Nrf2/ARE signalling by increasing nuclear localisation, DNA binding and transcriptional activity of Nrf2, as well as increasing protein levels of HO-1 and NQO1. Suppression of Nrf2 activity through siRNA or with the use of trigonelline resulted in the loss of anti-inflammatory activity by thymoquinone. Taken together, our studies show that thymoquinone inhibits NF-κB-dependent neuroinflammation in BV2 microglia, by targeting antioxidant pathway involving activation of both Nrf2/ARE. We propose that activation of Nrf2/ARE signalling pathway by thymoquinone probably results in inhibition of NF-κB-mediated neuroinflammation.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Velagapudi R,Kumar A,Bhatia HS,El-Bakoush A,Lepiarz I,Fiebich BL,Olajide OA

doi

10.1016/j.intimp.2017.04.018

subject

Has Abstract

pub_date

2017-07-01 00:00:00

pages

17-29

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(17)30152-2

journal_volume

48

pub_type

杂志文章

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