Open AccessLinalyl acetate prevents hypertension-related ischemic injury
Author(s) -
Yu Shan Hsieh,
Sae-Hyuk Kwon,
Hui Su Lee,
Geun Hee Seol
Publication year - 2018
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0198082
Subject(s) - nicotinamide adenine dinucleotide phosphate , reactive oxygen species , medicine , pharmacology , nadph oxidase , nitric oxide , oxidative stress , ischemia , in vivo , endocrinology , chemistry , oxidase test , biochemistry , biology , enzyme , microbiology and biotechnology
Ischemic stroke remains an important cause of disability and mortality. Hypertension is a critical risk factor for the development of ischemic stroke. Control of risk factors, including hypertension, is therefore important for the prevention of ischemic stroke. Linalyl acetate (LA) has been reported to have therapeutic effects in ischemic stroke by modulating intracellular Ca 2+ concentration and having anti-oxidative properties. The preventive efficacy of LA has not yet been determined. This study therefore investigated the preventive efficacy of LA in rat aortas exposed to hypertension related-ischemic injury, and the mechanism of action of LA.Hypertension was induced in vivo following ischemic injury to the aorta induced by oxygen-glucose deprivation and reoxygenation in vitro . Effects of LA were assayed by western blotting, by determining concentrations of lactate dehydrogenase (LDH) and reactive oxygen species (ROS) and by vascular contractility assays. LA significantly reduced systolic blood pressure in vivo . In vitro , LA suppressed ischemic injury-induced expression of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit p47 phox , as well as ROS production, LDH release, and ROS-induced endothelial nitric oxide synthase suppression. These findings indicate that LA has anti-hypertensive properties that can prevent hypertension-related ischemic injury and can prevent NADPH oxidase-induced production of ROS.