Affiliation:
1. Department of Cardiology, the Affiliated Hospital of Qingdao University, No. 16 Jiangsu Road, Qingdao 266003, Shandong, People’s Republic of China.
2. Department of Cardiology, Qingdao Third People’s Hospital, Qingdao 266041, Shandong, People’s Republic of China.
3. Department of Internal Medicine, Qingdao Commercial Hospital, Qingdao 266011, Shandong, People’s Republic of China.
Abstract
This study aimed to study the combined effect of rosuvastatin and probucol on atherosclerosis (AS) in rats. In total, 95 male Wistar rats were divided into 5 groups: 25 in the control group (A), 25 in the model group (B), 15 in the rosuvastatin group (C), 15 in the probucol group (D), and 15 in the rosuvastatin combined probucol group (E). A high-lipid diet and vitamin D3 were administered to establish AS rat model. Groups C, D, and E received corresponding drugs. Blood lipids, oxidized low-density lipoprotein (OX-LDL), malonaldehyde (MDA), superoxide dismutase (SOD), adiponectin (APN), and vascular endothelial cadherin (VE-cadherin) were measured. Platelet endothelial cell adhesion molecule-1 (PECAM-1) was detected by immune histochemistry. In groups B–E, AS rat models were successfully constructed. In groups C–E, blood lipids, OX-LDL, VE-cadherin, MDA, PECAM-1, and intimal thickness were decreased (p < 0.01), while SOD and APN were increased (p < 0.05), compared with that in group B. Furthermore, group E had lower levels of OX-LDL, MDA, and PECAM-1 but higher levels of SOD and APN and attenuated intimal thickening compared with groups C or D (p < 0.05). Administering rosuvastatin and probucol could attenuate AS lesions through modulation of oxidative stress, PECAM-1, and APN. Both drugs might help slow the progression of AS.
Publisher
Canadian Science Publishing
Subject
Physiology (medical),Pharmacology,General Medicine,Physiology
Cited by
12 articles.
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