The effects of atorvastatin on antioxidant/antiinflammatory propertiesof HDLs in hypercholesterolemics

Abstract

Background/aim: Hypercholesterolemia is characterized by changes in lipid profile, nitric oxide pathway, and oxidative stress markers, but functions of high-density lipoprotein (HDL) were not well established in hypercholesterolemic subjects treated with atorvastatin. In this study, we aimed to evaluate effects of atorvastatin treatment on functionality of HDL, oxidative stress, and endothelial functions in hypercholesterolemic subjects. Materials and methods:Thirty patients (20 females, 10 males) aged from 40 to 60 years and diagnosed as hypercholesterolemic were included. Patients were treated with 10 mg/day atorvastatin for 3 months. Markers of endothelial functions, namely asymmetric dimethylarginine (ADMA), homocysteine, and nitric oxide (NO), and markers of oxidative status, namely malondialdehyde (MDA), antioxidant potential (AOP), paraoxonase 1 (PON1), and arylesterase, were measured. Before and after atorvastatin treatment, glucose, lipid parameters, and antioxidant/antiinflammatory HDL levels were also measured.Results: ADMA and homocysteine levels were decreased whereas NO levels were increased with atorvastatin therapy. MDA levels were decreased but AOP, PON1, and arylesterase levels and antiinflammatory characteristics of HDLs were increased. Furthermore, lipid profiles of the patients improved with atorvastatin therapy. Conclusion:Hypercholesterolemia is a cause of oxidative stress, endothelial dysfunction, and proinflammatory HDL levels. Atorvastatin is a beneficial pharmacological modulator of impaired antiinflammatory HDL-C levels, endothelial functions, and oxidative status against atherosclerosis indicating pleiotropic effects of statins.

High‐density lipoprotein‐associated paraoxonase‐1 activity for prediction of adverse outcomes in outpatients with chronic heart failure

“…However, no factor was associated with increased ArylE activity on follow‐up. Several other studies have shown an increase in ArylE activity after statin treatment; however, only one was a randomized control study . Since diminished PON‐1 activity is linked to adverse outcomes in patients with HF, targeting those with diminished PON‐1 activity may provide a protective role in HF.…”

Modulation of Nitric Oxide Synthases by Oxidized LDLs: Role in Vascular Inflammation and Atherosclerosis Development

“…Consistent data show that the basal release of NO and the subsequent endothelial-dependent vasodilation are impaired during the development of hypercholesterolemia [11,12,13,14]. In particular, it has been assessed that local NO release is attenuated in patients undergoing serum levels of LDL up to 160 mg/dL [15,16].…”

Mutual Influences between Nitric Oxide and Paraoxonase 1

“…In any case, extracting a clinically applicable conclusion is highly speculative, and the often contradictory results on PON1 activity exerted by statins reported in different studies could be explained by the existence of gene polymorphisms among individuals. These would make some patients have higher PON1 levels so they might obtain further benefit from the treatment [65,66].…”

“…The protective effect of statins on endothelial function involves increasing NO biosynthesis and bioavailability via the direct up-regulation of eNOS expression [67]. In contrast to the above-mentioned study of Çiftci et al [65], where atorvastatin behaved as a beneficial pharmacological modulator of impaired endothelial functions by decreasing ADMA levels, some other studies to date indicated that statins have no or little effect on ADMA levels [68,69].…”