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Year : 2021  |  Volume : 64  |  Issue : 2  |  Page : 88-96

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

1 Department of Basic Nursing Science, School of Nursing, Korea University, Seoul, Republic of Korea; Department of Nursing, School of Nursing, National Taipei University of Nursing and Health Sciences, Taipei, Taiwan
2 Department of Basic Nursing Science, School of Nursing, Korea University, Seoul, Republic of Korea
3 Department of Basic Nursing Science, School of Nursing; BK21 FOUR Program of Transdisciplinary Major in Learning Health Systems, Graduate School, Korea University, Seoul, Republic of Korea

Correspondence Address:
Prof. Geun Hee Seol
Department of Basic Nursing Science, College of Nursing, Korea University, 145 Anam-ro, Seongbuk-gu, Seoul 02841
Republic of Korea
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/cjp.cjp_94_20

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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 p47phox expression in the human SH-SY5Y neural-like cells; decreased NOX2 expression and ROS generation in the BV2 murine microglial cells; and reduced p47phox expression 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. We found that LA exerted a protective effect in the BEND cells that may differ from its protective effects in other NVU cell types, following OGD/R-induced damage in the context of elevated [Ca2+]o.

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