Effects of dihydropyridine calcium channel blockers on oxidized low-density lipoprotein induced proliferation and oxidative stress of vascular smooth muscle cells

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• 作者：Jun Zou (1)
  Yan Li (1)
  Hong-Qi Fan (1)
  Ji-Guang Wang (1)
  
• 关键词：Calcium channel blockers ; Oxidative stress ; Oxidized low ; density lipoprotein ; Proliferation ; Vascular smooth muscle cells
• 刊名：BMC Research Notes
• 出版年：2012
• 出版时间：December 2012
• 年：2012
• 卷：5
• 期：1
• 全文大小：322KB
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• 作者单位：Jun Zou (1)
  Yan Li (1)
  Hong-Qi Fan (1)
  Ji-Guang Wang (1)
  
  1. Centre for Epidemiological Studies and Clinical Trials, The Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Ruijin 2nd Road 197, Shanghai, 200025, China
  

文摘

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.