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Antioxidant effects of statins in patients with atherosclerotic cerebrovascular disease
Gyeong Joon Moon1, Suk Jae Kim2, Yeon Hee Cho3
1Medical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Korea. ; Clinical Research Center, Samsung Biomedical Research Institute, Seoul, Korea.
Insights
High-dose statin use reduced oxidative stress markers like malondialdehyde (MDA) and oxidized low-density lipoprotein (oxLDL) in atherosclerotic stroke patients. However, effects on protein and DNA oxidation were not observed, indicating statins target lipid peroxidation.
Area of Science:
- Neurology
- Cardiology
- Biochemistry
Background:
- Oxidative stress contributes to stroke pathophysiology and brain injury.
- Statins offer pleiotropic and lipid-lowering benefits, with high doses reducing cerebrovascular event risk.
- Data on oxidative stress marker changes post-statin in atherosclerotic stroke is limited.
Purpose of the Study:
- To evaluate changes in oxidative stress markers after short-term high-dose statin use in atherosclerotic stroke patients.
- To assess the impact of statins on lipid, protein, and DNA oxidation markers.
Main Methods:
- 99 atherosclerotic stroke patients received 20 mg/day rosuvastatin for one month.
- Serum levels of malondialdehyde (MDA), oxidized LDL (oxLDL), protein carbonyl content (PCO), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were measured pre- and post-treatment.
Main Results:
- Statin use significantly decreased MDA and oxLDL levels (p<0.05).
- MDA and PCO levels correlated with infarct volumes.
- OxLDL reduction was linked to decreased cholesterol, LDL, and apolipoprotein B.
Conclusions:
- Short-term statin use shows antioxidant effects against lipid peroxidation in atherosclerotic stroke.
- Mechanisms include both lipid-lowering dependent and independent pathways.
- Statins did not significantly affect protein or DNA oxidation markers in this cohort.
Background And Purpose:
Oxidative stress is involved in the pathophysiological mechanisms of stroke (e.g., atherosclerosis) and brain injury after ischemic stroke. Statins, which inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, have both pleiotropic and low-density lipoprotein (LDL)-lowering properties. Recent trials have shown that high-dose statins reduce the risk of cerebrovascular events. However, there is a paucity of data regarding the changes in the oxidative stress markers in patients with atherosclerotic stroke after statin use. This study evaluated changes in oxidative stress markers after short-term use of a high-dose statin in patients with atherosclerotic stroke.
Methods:
Rosuvastatin was administered at a dose of 20 mg/day to 99 patients who had suffered an atherosclerotic stroke and no prior statin use. Blood samples were collected before and 1 month after dosing, and the serum levels of four oxidative stress markers-malondialdehyde (MDA), oxidized LDL (oxLDL), protein carbonyl content (PCO), and 8-hydroxy-2'-deoxyguanosine (8-OHdG)-were evaluated to determine the oxidation of MDA and lipids, proteins, and DNA, respectively, at both of those time points.
Results:
The baseline levels and the degrees of reduction after statin use differed among the oxidative stress markers measured. MDA and PCO levels were associated with infarct volumes on diffusion-weighted imaging (r=0.551, p<0.05, and r=0.444, p=0.05, respectively). Statin use decreased MDA and oxLDL levels (both p<0.05) but not the PCO or 8-OHdG level. While the reduction in MDA levels after statin use was not associated with changes in cholesterol, that in oxLDL levels was proportional to the reductions in cholesterol (r=0.479, p<0.01), LDL (r=0.459, p<0.01), and apolipoprotein B (r=0.444, p<0.05).
Conclusions:
The impact of individual oxidative stress markers differs with time after ischemic stroke, suggesting that different oxidative markers reflect different aspects of oxidative stress. In addition, short-term use of a statin exerts antioxidant effects against lipid peroxidation via lipid-lowering-dependent and -independent mechanisms, but not against protein or DNA oxidation in atherosclerotic stroke patients.
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