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Biomed Pharmacother. 2016 Oct;83:635-640. doi: 10.1016/j.biopha.2016.07.018. Epub 2016 Jul 25.

Thymoquinone: An edible redox-active quinone for the pharmacotherapy of neurodegenerative conditions and glial brain tumors. A short review.

Author information

1
Department of Neurosurgery, Memorial Hospital, Istanbul, Turkey.
2
Department of Immunology, Istanbul University-DETAE, Istanbul, Turkey. Electronic address: maltinoz@gmail.com.

Abstract

There exist few efficient agents in the neurological and neurosurgical armamentarium for treatment of neurotrauma, refractory seizures and high grade glial tumors. Pathophysiological conditions of diverse neural injuries have converging common pathways including oxidative stress and apoptosis. Targeted therapies have been throughly investigated, but limited success has been achieved until now. Phytochemical drugs may provide easily achievable and cheap adjunctive sources. Thymoquinone is an edible quinone obtained from Nigella sativa seed oil and exerts powerful antiinflammatory, antioxidant and antitumor activities in experimental models. Recently emerging studies conducted with animal models suggest that thymoquinone - bearing a very simple molecular structure - significantly crosses the blood brain barrier and exerts neuromodulatory activities. Indeed, in animal studies, the following actions of thymoquinone were demonstrated: 1-Protection against ischemic brain damage. 2-Reduction of epileptic seizures and associated cerebral oxidative injury. 3-Reduction of morphine tolerance and associated oxidative brain damage. 4-Anxiolytic effects and reduction of immobility stress-associated cerebral oxidative injury. 5-Reduction of diabetes-induced cerebral oxidative stress, 6-Reduction of cerebral oxidative injuries induced by noxious exposures including toluene, lead and ionizing radiation. Substantial in vitro data suggest that thymoquinone may be beneficial in treatment of glial tumors. However, there is no clinical study investigating its antitumor effects. In fact, thymoquinone suppresses growth and invasion, and induces apoptosis of glial tumor cells via degrading tubulins and inhibiting 20S proteasome, telomerase, autophagy, FAK and metalloproteinases. A simple and easily available agent may be a promising adjunctive treatment option in neurological and neurosurgical practice.

KEYWORDS:

Glial tumor; Glioblastoma; Neurodegenerative disease; Oxidative injury; Thymoquinone

PMID:
27459120
DOI:
10.1016/j.biopha.2016.07.018
[Indexed for MEDLINE]

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