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Background: Rosuvastatin is a cholesterol-lowering medication that also reduces the production of superoxide anion, which reduces inflammation and oxidative stress. In the mitochondria, manganese-dependent superoxide dismutase (MnSOD or SOD2) is responsible for the metabolization of superoxide anions. A gene polymorphism in humans (Ala16Val-SOD2) causes the 16th amino acid of alanine (Ala) to become valine (Val). Due to their pro-inflammatory effects and increased oxidative stress, functional polymorphisms of these antioxidant enzymes are thought to play a role in the pathogenesis of CAD. In this study, we looked at how rosuvastatin affected inflammation and oxidative stress in hypertensive and dyslipidemic patients.
Methods: We looked at the antioxidant profile of the SOD2 gene V16A polymorphism in 51 CAD patients who were taking 10 mg of rosuvastatin daily. During the study, the following variables were recorded: age, weight, BMI, blood pressure, SOD2(superoxide dismutase 2), and MDA: malondialdehyde, glutathione peroxidase (Gpx), lipoprotein lipase (LPL), and interleukin 6 (IL6) AL-Sadar and AL-Hakeem Hospitals & Research Center, as well as the university of kufa's faculty of pharmacy, were the locations of this study. Different statistical analyses were carried out.
Result: SOD2 genes were found to have significantly different distributions of alleles and genotypes in people with CAD. Rosuvastatin had a significant positive effect as an anti-inflammatory medication in CAD patients by elevated serum SOD2 antioxidant levels.
Conclusion: This study demonstrates that oxidative stress in CAD can be accelerated not only by hyperlipidemia-induced ROS production but also by a diminished antioxidant defense system, at least partially caused by SOD2 SNPs. Rosuvastatin reduced that oxidative stress and inflammation. These results show that there is an additional cardio protective effect, which could be a pleiotropic effect or a direct mechanism of action.
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