Protection of the neurovascular unit from calcium-related ischemic injury by linalyl acetate

Yu Hsieh, You Shin, Geun Seol

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)


Calcium-related ischemic injury (CRII) can damage cells of the neurovascular unit (NVU). Here, we investigate the protective effects of linalyl acetate (LA) against CRII-induced NVU damage and evaluate the underlying mechanisms. The protective effects of LA in cell lines representative of NVU components (BEND, SH-SY5Y, BV2, and U373 cells) were evaluated following exposure to oxygen-glucose deprivation/reoxygenation alone (OGD/R-only) or OGD/R in the presence of 5 mM extracellular calcium ([Ca2+]o) to mimic CRII. LA reversed damage under OGD/R-only conditions by blocking p47phox/NADPH oxidase (NOX) 2 expression, reactive oxygen species (ROS) production, nitric oxide (NO) abnormality, and lactate dehydrogenase (LDH) release only in the BEND cells. However, under CRII-mimicking conditions, LA reversed NO abnormality and matrix metalloproteinase (MMP)-9 activation in the BEND murine brain endothelial cells; inhibited p47phoxexpression in the human SH-SY5Y neural-like cells; decreased NOX2 expression and ROS generation in the BV2 murine microglial cells; and reduced p47phoxexpression in the U373 human astrocyte-like cells. Importantly, LA protected against impairment of the neural cells, astrocytes, and microglia, all of which are cellular components of the NVU induced by exposure to CRII-mimicking conditions, by reducing LDH release.

Original languageEnglish
Pages (from-to)88-96
Number of pages9
JournalChinese Journal of Physiology
Issue number2
Publication statusPublished - 2021 Mar 1

Bibliographical note

Publisher Copyright:
© 2021 Wolters Kluwer Medknow Publications. All rights reserved.


  • Calcium-related ischemic injury
  • linalyl acetate
  • neurovascular unit

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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