Rosuvastatin effects on systemic oxidative stress, endogenous inflammation and main neoangiogenesis factors in patients with atherosclerosis
Aim. To investigate rosuvastatin effects on oxidative stress (OS), endogenous inflammation and neoangiogenesis process in patients with systemic atherosclerosis (SA).Material and methods. In total, 46 SA patients (mean age 56,5±2,2 years) were divided into two groups, comparable by clinical and func...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | Russian |
| Published: |
«SILICEA-POLIGRAF» LLC
2009-08-01
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| Series: | Кардиоваскулярная терапия и профилактика |
| Subjects: | |
| Online Access: | https://cardiovascular.elpub.ru/jour/article/view/1811 |
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| Summary: | Aim. To investigate rosuvastatin effects on oxidative stress (OS), endogenous inflammation and neoangiogenesis process in patients with systemic atherosclerosis (SA).Material and methods. In total, 46 SA patients (mean age 56,5±2,2 years) were divided into two groups, comparable by clinical and functional parameters. Group I (n=24) received standard therapy, while Group II (n=22) was administered standard therapy plus rosuvastatin (10 mg/d). In all participants, serum lipid profile, in vitro Cu-ion oxidation of serum and high-density lipoproteins (HDL), concentrations of 3-nitrotyrosine (3-NT), high-sensitive C-reactive protein (hs-CRP), and interleukin-6 (IL-6), activity of secretory phospholipase A2 Type IIA (secPHLA2-IIA), and VEGF and PIGF factor levels were measured.Results. Moderate doses of rosuvastatin significantly decreased serum and HDL oxidation — by 34% (р<0,01) and 37% (р<0,05), respectively. They also reduced the levels of 3-NT by 26% (р<0,05), hs-CRP — by 35% (р<0,05), and IL-6 — 26% (р<0,05). SecPHLA2-IIA activity decreased by 27% (р<0,05), VEGF level — by 28% (р<0,05), and PIGF level - by 43,5% (р<0,05).Conclusion. 3-NT and hs-CRP levels, together with secPHLA2-IIA activity, could be effective markers of systemic OS and endogenous inflammation in SA patients. |
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| ISSN: | 1728-8800 2619-0125 |