Jump to main content
US EPA
United States Environmental Protection Agency
Search
Search
Main menu
Environmental Topics
Laws & Regulations
About EPA
Health & Environmental Research Online (HERO)
Contact Us
Print
Feedback
Export to File
Search:
This record has one attached file:
Add More Files
Attach File(s):
Display Name for File*:
Save
Citation
Tags
HERO ID
5672769
Reference Type
Journal Article
Title
Effects of dihydropyridine calcium channel blockers on oxidized low-density lipoprotein induced proliferation and oxidative stress of vascular smooth muscle cells
Author(s)
Zou, J; Li, Y; Fan, HQ; Wang, JG
Year
2012
Is Peer Reviewed?
Yes
Journal
BMC Research Notes
ISSN:
1756-0500
Book Title
BMC Res Notes. 2012, Jul 06; 5:168. [BMC research notes]
Volume
5
Language
English
DOI
10.1186/1756-0500-5-168
Abstract
BACKGROUND: Dihydropyridine calcium channel blockers (CCBs) are more effective in reducing carotid intima-media thickness (IMT) than other classes of antihypertensive drugs due to their vascular effects. However, the mechanism remains to be elucidated. FINDINGS: Ox-LDL induced HUVSMCs proliferation in a time- and dose-dependent manner. When pretreated with three CCBs before 50 μg/ml ox-LDL stimulation, 30 μM lacidipine and 3 μM amlodipine exhibited 27% and 18% decrease of pro-proliferative effect induced by ox-LDL, whereas (S-)-amlodipine did not have any anti-proliferative effect. 30 μM lacidipine inhibited about two-thirds of the ox-LDL induced ROS production in HUVSMCs, whereas amlodipine and (S-)-amlodipine did not have influence on ROS production. The MAPKs pathway inhibitors inhibited the ox-LDL induced proliferation of HUVSMCs. CONCLUSION: Our study has demonstrated that lipophilic CCBs, such as lacidipine may inhibit ox-LDL induced proliferation and oxidative stress of VSMCs, and that the ROS-MAPKs pathway might be involved in the mechanism.
Keywords
Amlodipine/pharmacology; Anthracenes/pharmacology; Butadienes/pharmacology; Calcium Channel Blockers/pharmacology; Cell Proliferation/drug effects; Cells, Cultured; Dihydropyridines/pharmacology; Dose-Response Relationship, Drug; Imidazoles/pharmacology; JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism; Lipoproteins, LDL/pharmacology; MAP Kinase Signaling System/drug effects; Muscle, Smooth, Vascular/cytology; Myocytes, Smooth Muscle/drug effects/metabolism; Nitriles/pharmacology; Oxidative Stress/drug effects; Pyridines/pharmacology; Reactive Oxygen Species/metabolism; Time Factors; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism; 1J444QC288; 1TW30Y2766; 260080034N
Home
Learn about HERO
Using HERO
Search HERO
Projects in HERO
Risk Assessment
Transparency & Integrity