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

Velagapudi, Ravikanth, Kumar, Asit, Bhatia, Harsharan S., El-Bakoush, Abdelmeneim, Lepiarz, Izabela, Fiebich, Bernd L and Olajide, Olumayokun A (2017) Inhibition of neuroinflammation by thymoquinone requires activation of Nrf2/ARE signalling. International Immunopharmacology, 48. pp. 17-29. ISSN 1567-5769

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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-B 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-kappaB-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-kappaB-mediated neuroinflammation.

Item Type: Article
Subjects: R Medicine > RM Therapeutics. Pharmacology
Schools: School of Applied Sciences
Related URLs:
Depositing User: Olumayokun Olajide
Date Deposited: 25 Apr 2017 10:02
Last Modified: 21 Jun 2017 16:56
URI: http://eprints.hud.ac.uk/id/eprint/31763

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