Ethanol promotes rat aortic vascular smooth muscle cell proliferation via increase of homocysteine and oxidized-low-density lipoprotein
Autor: | Behrouz Ilkhanizadeh, Naseh Abdollahzadeh, Alireza Shirpoor, Mohammad-Hasan Khadem Ansari, Siamak Salami |
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Rok vydání: | 2013 |
Předmět: |
Male
medicine.medical_specialty Vascular smooth muscle Time Factors Homocysteine Alcohol Drinking Cell medicine.disease_cause Muscle Smooth Vascular chemistry.chemical_compound Risk Factors Internal medicine medicine Animals Rats Wistar Aorta Cell Proliferation Ethanol medicine.diagnostic_test business.industry Cell growth Atherosclerosis Rats Lipoproteins LDL Oxidative Stress medicine.anatomical_structure Endocrinology chemistry Vascular smooth muscle cell cardiovascular system Rat Oxidized-low-density lipoprotein Lipid profile business Cardiology and Cardiovascular Medicine Oxidative stress Lipoprotein |
Zdroj: | Journal of Cardiology. 62(6):374-378 |
ISSN: | 0914-5087 |
DOI: | 10.1016/j.jjcc.2013.06.003 |
Popis: | Background Increased levels of homocysteine and oxidized low-density lipoprotein (Ox-LDL) are considered independent risk factors for atherosclerosis. However, no previous study has examined the effects of ethanol-induced increase of homocysteine and Ox-LD on aortic vascular smooth muscle cell (VSMC) proliferation. The aim of the present study was to investigate the relationship between ethanol consumption, increase in homocysteine, Ox-LDL, and aortic VSMC proliferation in rats. Methods and results To address this issue, 24 male Wistar rats were randomly divided into three groups: control, sham, and ethanol-treated. Homocysteine, Ox-LDL, lipid profile, and aortic VSMC proliferation were assessed after 42 days. The results revealed a concurrent, significant increase in homocysteine and Ox-LDL levels, lipid profile levels, and aortic VSMC proliferation in the ethanol-treated group compared with the control and sham groups. Conclusion Based on these results, we conclude that ethanol apparently exerts aortic VSMC proliferation through increase in homocysteine and Ox-LDL-mediated oxidative stress, which in turn trigger proatherogenic changes in the aortic wall. |
Databáze: | OpenAIRE |
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