PMID- 33938819
OWN - NLM
STAT- MEDLINE
DCOM- 20210505
LR  - 20210505
IS  - 0304-4920 (Print)
IS  - 0304-4920 (Linking)
VI  - 64
IP  - 2
DP  - 2021 Mar-Apr
TI  - Protection of the neurovascular unit from calcium-related ischemic injury by 
      linalyl acetate.
PG  - 88-96
LID - 10.4103/cjp.cjp_94_20 [doi]
AB  - 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 ([Ca(2+)](o)) to mimic CRII. LA reversed damage under 
      OGD/R-only conditions by blocking p47(phox)/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 p47(phox) expression in the human SH-SY5Y neural-like cells; decreased 
      NOX2 expression and ROS generation in the BV2 murine microglial cells; and 
      reduced p47(phox) 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 [Ca(2+)](o).
FAU - Hsieh, Yu Shan
AU  - Hsieh YS
AD  - 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.
FAU - Shin, You Kyoung
AU  - Shin YK
AD  - Department of Basic Nursing Science, School of Nursing, Korea University, Seoul, 
      Republic of Korea.
FAU - Seol, Geun Hee
AU  - Seol GH
AD  - 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.
LA  - eng
PT  - Journal Article
PL  - India
TA  - Chin J Physiol
JT  - The Chinese journal of physiology
JID - 7804502
RN  - 0 (Monoterpenes)
RN  - 0 (Reactive Oxygen Species)
RN  - 5K47SSQ51G (linalyl acetate)
RN  - IY9XDZ35W2 (Glucose)
RN  - S88TT14065 (Oxygen)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - *Calcium
MH  - *Endothelial Cells
MH  - Glucose
MH  - Humans
MH  - Mice
MH  - Monoterpenes
MH  - Oxygen
MH  - Reactive Oxygen Species
OTO - NOTNLM
OT  - Calcium-related ischemic injury
OT  - linalyl acetate
OT  - neurovascular unit
COIS- None
EDAT- 2021/05/04 06:00
MHDA- 2021/05/06 06:00
CRDT- 2021/05/03 12:34
PHST- 2021/05/03 12:34 [entrez]
PHST- 2021/05/04 06:00 [pubmed]
PHST- 2021/05/06 06:00 [medline]
AID - ChinJPhysiol_2021_64_2_88_315093 [pii]
AID - 10.4103/cjp.cjp_94_20 [doi]
PST - ppublish
SO  - Chin J Physiol. 2021 Mar-Apr;64(2):88-96. doi: 10.4103/cjp.cjp_94_20.