Curcumin attenuates blood-brain barrier disruption after subarachnoid hemorrhage in mice

Abstract Background Early brain injury (EBI), one of the most important mechanisms underlying subarachnoid hemorrhage (SAH), comprises edema formation and blood-brain barrier (BBB) disruption. Curcumin, an active extract from the rhizomes of Curcuma longa, alleviates neuroinflammation by as yet unkn...

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Veröffentlicht in:The Journal of surgical research 2017-01, Vol.207, p.85-91
Hauptverfasser: Yuan, Jichao, Liu, Wei, Zhu, Haitao, Zhang, Xuan, Feng, Yang, Chen, Yaxing, Feng, Hua, Lin, Jiangkai
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Sprache:eng
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Zusammenfassung:Abstract Background Early brain injury (EBI), one of the most important mechanisms underlying subarachnoid hemorrhage (SAH), comprises edema formation and blood-brain barrier (BBB) disruption. Curcumin, an active extract from the rhizomes of Curcuma longa, alleviates neuroinflammation by as yet unknown neuroprotective mechanisms. In this study, we examined whether curcumin treatment ameliorates SAH-induced brain edema and BBB permeability changes, as well as the mechanisms underlying this phenomenon. Methods We induced SAH in mice via endovascular perforation, administered curcumin 15 mins after surgery and evaluated neurological scores, brain water content, Evans blue extravasation, Western blot assay results and immunohistochemical analysis results 24 hours after surgery. Results Curcumin significantly improved neurological scores and reduced brain water content in treated mice compared with SAH mice. Furthermore, curcumin decreased Evans blue extravasation, matrix metallopeptidase (MMP)-9 expression, and the number of Iba-1-positive microglia in treated mice compared with SAH mice. Lastly, curcumin treatment increased the expression of the tight junction (TJ) proteins zonula occludens-1 (ZO-1) and Occludin in treated mice compared with vehicle-treated and sample SAH mice. Conclusion We demonstrated that curcumin inhibits microglial activation and MMP-9 expression, thereby reducing brain edema and attenuating post-SAH BBB disruption in mice.
ISSN:0022-4804
1095-8673
DOI:10.1016/j.jss.2016.08.090