83 0

Amlodipine besylate and amlodipine camsylate prevent cortical neuronal cell death induced by oxidative stress

Title
Amlodipine besylate and amlodipine camsylate prevent cortical neuronal cell death induced by oxidative stress
Author
이규용
Keywords
amlodipine besylate; amlodipine camsylate; calcium channel blocker; neuroprotection; oxidative stress; phosphatidylinositol 3-kinase; HYDROGEN-PEROXIDE PRODUCTION; ACUTE ISCHEMIC-STROKE; CALCIUM-ANTAGONISTS; SIGNALING PATHWAY; 3-KINASE PATHWAY; CONTROLLED TRIAL; OPEN-LABEL; DAMAGE; NIMODIPINE; PHOSPHORYLATION
Issue Date
2011-09
Publisher
WILEY-BLACKWELL, COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
Citation
JOURNAL OF NEUROCHEMISTRY, Vol.119, No.6 [2011], p1262-1270
Abstract
We examined the neuroprotective effects of the long-acting third-generation dihydropyridine Ca2+ antagonists, amlodipine besylate (AB) and amlodipine camsylate (AC), on neuronal cell death induced by oxidative stress. Cell viability and levels of free radicals and intracellular signaling proteins were measured after treating primary cultures of cortical neurons with AB, AC, and/or hydrogen peroxide (H2O2) under various conditions. Cell viability was not affected by concentrations of AB or AC up to 5 mu M but decreased at higher concentrations. Following H2O2 exposure, the viability of cortical neurons decreased in a concentration-dependent manner; however, treatment with AB or AC up to 5 mu M restored the viability of H2O2-injured cortical neurons. Treatment with H2O2 increased the level of free radicals in cortical neurons, and pre-treatment with AB or AC counteracted this in a dose-dependent manner. Similarly, treatment with AB or AC reduced the declines in p85aPI3K, phosphorylated Akt, phosphorylated GSK-3 beta, heat-shock transcription factor-1, and Bcl-2 induced by H2O2, as well as the increases in cyclooxygenase-2, cytosolic cytochrome c, cleaved caspase 9, and cleaved caspase 3. Our results indicate that AB and AC exert similar neuroprotective effects by reducing oxidative stress, enhancing survival signals, and inhibiting death signals.
URI
http://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2011.07529.x/abstracthttp://hdl.handle.net/20.500.11754/36468
ISSN
0022-3042
DOI
10.1111/j.1471-4159.2011.07529.x
Appears in Collections:
COLLEGE OF MEDICINE[S](의과대학) > MEDICINE(의학과) > Articles
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE