The association of therapeutic responses of rosuvastatin with the superoxide dismutase 2 enzyme gene polymorphism in coronary artery disease patients at najaf governorate
Keywords:
coronary artery disease, oxidative stress, SOD2 gene V16A polymorphism, PCR- RFLP, lipoproteins, cholesterolAbstract
Background: One of the most consistent hypotheses to explain atherogenesis postulates and reported to be involved in the pathogenesis of CAD is triggered by LDL oxidation caused by Superoxide anions. Rosuvastatin is a drug that lowers cholesterol, but it is now thought to improve cardiovascular morbidity and mortality through pleiotropic effects arising from their antioxidant, anti-inflammatory, and antiplatelet properties. In the mitochondria, manganese-dependent superoxide dismutase (MnSOD or SOD2) metabolizes the superoxide anions. A gene polymorphism in humans (Ala16Val-SOD2) causes the 16th amino acid of alanine (Ala) to become valine (Val).
Methods: We examined the lipid profile and SOD2 gene V16A polymorphism in 51 CAD patients who were on rosuvastatin 10 mg/day. During the investigation, the following factors were noted: Age, weight, BMI, blood pressure, TG (triglyceride), LDL (low density lipoprotein), HDL (high density lipoprotein), VLDL (very low density lipoprotein), and SOD2 (superoxide dismutase) are some of the variables that are taken into consideration. The AL- Sadar and AL-Hakeem Hospitals & Research Centre, the university of Kufa's pharmacy faculty, and other locations participated in this investigation. Several statistical analyses were used.
Result: SOD2 genes showed significant changes in allele and genotype distribution across CAD patients. After using rosuvastatin, serum ldl levels in CAD participants considerably fell.
Conclusion: The findings of this study show that Rosuvastatin decreased inflammation and oxidative stress in CAD and increased the capability of the antioxidant defense system, which was at least partially triggered by SNPs of SOD2. This improved the lipid profile in hyperlipidemia. These findings show the existence of an extra cardioprotective effect, which may be a pleiotropic effect or arise from a direct mechanism of action.
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