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Molecular Biology Reports

, Volume 46, Issue 1, pp 241–250 | Cite as

Allyl isothiocyanate attenuates oxidative stress and inflammation by modulating Nrf2/HO-1 and NF-κB pathways in traumatic brain injury in mice

  • Berrak Caglayan
  • Ertugrul Kilic
  • Arman Dalay
  • Serdar Altunay
  • Mehmet Tuzcu
  • Fusun Erten
  • Cemal Orhan
  • Mehmet Yalcin Gunal
  • Burak Yulug
  • Vijaya Juturu
  • Kazim SahinEmail author
Original Article

Abstract

Traumatic brain injury (TBI) is the leading cause of mortality and morbidity in young adults and children in the industrialized countries; however, there are presently no FDA approved therapies. TBI results in oxidative stress due to the overproduction of reactive oxygen species and overwhelming of the endogenous antioxidant mechanisms. Recently, it has been reported that antioxidants including phytochemicals have a protective role against oxidative damage and inflammation after TBI. To analyze the effects of a naturally occurring antioxidant molecule, allyl isothiocyanate (AITC), on the nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor kappa B (NF-κB) signaling pathways in TBI, a cryogenic injury model was induced in mice. Here, we showed that AITC administered immediately after the injury significantly decreased infarct volume and blood–brain barrier (BBB) permeability. Protein levels of proinflammatory cytokines interleukin-1β (IL1β) and interleukin-6 (IL6), glial fibrillary acidic protein (GFAP) and NF-κB were decreased, while Nrf2, growth-associated protein 43 (GAP43) and neural cell adhesion molecule levels were increased with AITC when compared with vehicle control. Our results demonstrated that the antioxidant molecule AITC, when applied immediately after TBI, provided beneficial effects on inflammatory processes while improving infarct volume and BBB permeability. Increased levels of plasticity markers, as well as an antioxidant gene regulator, Nrf2, by AITC, suggest that future studies are warranted to assess the protective activities of dietary or medicinal AITC in clinical studies.

Graphical abstract

Keywords

Traumatic brain injury Allyl isothiocyanate NF-κB Nrf2 

Abbreviations

AITC

Allyl isothiocyanate

BBB

Blood–brain barrier

GAP43

Growth-associated protein 43

GFAP

Glial fibrillary acidic protein

ICAM-1

Intercellular adhesion molecule-1

IL1β

Interleukin-1β

IL6

Interleukin-6

NCAM

Neural cell adhesion molecule

NF-κB

Nuclear factor kappa B

Nrf2

Nuclear factor erythroid 2-related factor 2

ROS

Reactive oxygen species

TBI

Traumatic brain injury

Notes

Acknowledgements

This study was supported by OmniActive Health Technologies Ltd. NJ, USA. This work was also supported in part by The Turkish Academy of Sciences (TUBA) (KS, EK).

Funding

This study was supported by OmniActive Health Technologies Inc. (NJ, USA). This work was also supported in part by the Turkish Academy of Sciences.

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

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Copyright information

© Springer Nature B.V. 2018

Authors and Affiliations

  1. 1.Department of Medical Biology, International School of MedicineIstanbul Medipol UniversityIstanbulTurkey
  2. 2.Department of PhysiologyIstanbul Medipol UniversityIstanbulTurkey
  3. 3.Regenerative and Restorative Medical Research CenterIstanbul Medipol UniversityIstanbulTurkey
  4. 4.Division of Biology, Faculty of ScienceFirat UniversityElazigTurkey
  5. 5.Animal Nutrition Department, School of Veterinary MedicineFirat UniversityElazigTurkey
  6. 6.Department of Neurology, School of MedicineIstanbul Medipol UniversityIstanbulTurkey
  7. 7.Research and DevelopmentOmniActive Health Technologies Inc.MorristownUSA

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