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The effects of rosuvastatin on lipid-lowering, inflammatory, antioxidant and fibrinolytics

blood biomarkers are influenced by Val16Ala superoxide dismutase manganese-dependent

gene polymorphism

Rosuvastatin is known for its effectiveness on making high cholesterol and triglycerides.
Conversely, it showed influence on oxidative stress. These effects are said to be related to
functional gene polymorphism involved in enzymatic antioxidant activities. Gene polymorphism
of Val16Ala-SOD2 is the root of upshot. This study corresponds to the polymorphism of
Val16Ala-SOD2 and its effect on the lowering of lipid profile, inflammatory, antioxidant and
fibrinolytics biomarkers on Rosuvastain, a cholesterol-lowering drug. In this study, 122
hypercholesterololemic individuals who haven't taken any pharmacological cholesterol-lowering
therapy, were subjected to observation, moreover, sex, age, and body mass index were taken into
consideration to see if they are also dependent on the results. Val16Ala-SOD2 genotyping
determination was performed via polymerase chain reaction by using a modification of Barbisan
et al s technique. A daily dose of 20-mg Rosuvastatin was given for 120-day therapy. Venous
puncture was administered before and after the therapy for laboratory anlaysis. In addition,
fasting glucose and serum total cholesterol, tiglyceride concentartions, high-density liproprotein,
LDL cholesterol, coagulation parameters, and several inflammatory metabolism biomarkers were
measured. SPSS and two-way variant analysis were conducted in order to compare the laboratory
results. The study has shown that the extent of the effect of Rosuvastatin is dependent on the
Val16Ala-SOD2. Patients who hasVV genotype are more resistant to the lipid lowering
Rosuvastatin therapy than those with the A-allele patients. A-allele patients are affected on the
inflammatory and fibrinolytic biomarkers.