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

Ravikanth Velagapudi, Asit Kumar, Harsharan S. Bhatia, Abdelmeneim El-Bakoush, Izabela Lepiarz, Bernd L. Fiebich, Olumayokun A. Olajide

Research output: Contribution to journalArticle

32 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)17-29
Number of pages13
JournalInternational Immunopharmacology
Volume48
Early online date3 May 2017
DOIs
Publication statusPublished - 1 Jul 2017

Fingerprint Dive into the research topics of 'Inhibition of neuroinflammation by thymoquinone requires activation of Nrf2/ARE signalling'. Together they form a unique fingerprint.

  • Cite this