期刊
CHINESE JOURNAL OF PHYSIOLOGY
卷 64, 期 2, 页码 88-96出版社
WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4103/cjp.cjp_94_20
关键词
Calcium-related ischemic injury; linalyl acetate; neurovascular unit
类别
资金
- Basic Science Research Program through the National Research Foundation of Korea [NRF-2018R1D1A1B07050048]
The study found that linalyl acetate (LA) has a protective effect on neural cells, astrocytes, and microglia damaged under conditions simulating CRII, reducing LDH release. The protective effects of LA on different NVU cell types may vary, involving mechanisms such as blocking oxidative stress and reducing nitric oxide abnormalities.
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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