Hydroquinone strongly alleviates focal ischemic brain injury via blockage of blood-brain barrier disruption in rats

Joon Ha Park, Ki Yeon Yoo, In Hye Kim, Jeong Hwi Cho, Jae Chul Lee, Ji Hyeon Ahn, Hyun Jin Tae, Bing Chun Yan, Dae Won Kim, Ok Kyu Park, Seung Hae Kwon, Song Her, Jin Su Kim, Jung Hoon Choi, Choong Hyun Lee, In Koo Hwang, Jae Youl Cho, Jun Hwi Cho, Young Guen Kwon, Sungwoo RyooYoung Myeong Kim, Moo Ho Won, Il Jun Kang

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)

Abstract

Hydroquinone (HQ), a major benzene metabolite, occurs naturally in various plants and is manufactured for commercial use. Although HQ displays various biological effects, its neuroprotective effects following ischemic insults have not been investigated. In this study, we first examined neuroprotective effects of HQ in a rat model of transient focal cerebral ischemia. Animals were subjected to transient middle cerebral artery occlusion for 120 min. HQ (50 or 100 mg/kg) or vehicle was intraperitoneally administered once at 30min after ischemia-reperfusion. Neuroprotection by treatment with 100 mg/kg of HQ was shown using evaluation of neurological deficits, positron-emission tomography (PET) and 2,3,5-triphenyltetrazoliumchloride (TTC) staining. In addition, HQ treatment significantly attenuated ischemia-induced Evans blue dye extravasation from blood vessels and significantly increased immunoreactivities of SMI-71 (an endothelial BBB marker) and glucose transporter-1 (GLUT-1, an endothelial cell marker) in ischemic cortex compared to the vehicle-treated ischemia-operated group. Confocal microscopy and western blot analysis also showed that HQ treatment maintained expressions of tight junction proteins (zonula occludens-1 and occludin) in the ischemic cortex. Post-treatment with HQ protected neurons from transient focal cerebral ischemic injury and the neuroprotective effect of HQ might be closely associated with prevention of BBB disruption via maintaining SMI-71 and GLUT-1 expressions as well as prevention of the degradation of zonula occludens-1 and occludin proteins.

Original languageEnglish
Pages (from-to)430-441
Number of pages12
JournalToxicological Sciences
Volume154
Issue number2
DOIs
Publication statusPublished - 2016

Bibliographical note

Funding Information:
This work was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT and future Planning (NRF-2014R1A2A2A01005307), by the Bio & Medical Technology Development Program of the NRF funded by the Korean government, MSIP (NRF-2015M3A9B6066835), and by the Bio-Synergy Research Project (NRF-2015M3A9C4076322) of the Ministry of Science, ICT and Future Planning through the National Research Foundation.

Publisher Copyright:
© The Author 2016. Published by Oxford University Press on behalf of Royal Society of Tropical Medicine and Hygiene. All rights reserved.

All Science Journal Classification (ASJC) codes

  • Toxicology

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