Interindividual variability of atorvastatin treatment influence on the MPO gene expression in patients after acute myocardial infarction.

Abstract

Myeloperoxidase (MPO) and C-reactive protein (CRP) may play critical roles in generation of oxidative stress and the development of the systemic inflammatory response. The aim of the study was to determine the effect of atorvastatin therapy on the MPO gene expression and its plasma level in relation to lipids level lowering and an anti-inflammatory response in patients after acute myocardial infarction. The research material was represented by 112 samples. Thirty-eight patients with first AMI receiving atorvastatin therapy (40 mg/day) and followed up for one month were involved in the study. The relative MPO gene expression in peripheral blood mononuclear cells (PBMCs) was examined using RT-qPCR in 38 patients before-, 38 patients after-therapy and in 36 patients as the control group. The plasma concentrations of MPO and serum concentrations of biochemical parameters were determined using commercially available diagnostic tests. After one month of atorvastatin therapy, in 60.5% patients a decrease of MPO gene expression, whereas in 39.5% patients an increase, was observed. The plasma MPO levels behaved in the same way as the MPO gene expression. However, the serum lipids and CRP concentrations were significantly lower after one month of atorvastatin therapy in both groups of patients -with decreased and increased MPO gene expression. Atorvastatin exhibited a different effect on MPO gene expression and its plasma level. Short-term atorvastatin therapy resulted in lipid lowering and anti-inflammatory activity in patients after AMI, independently of its effect on MPO gene expression. The molecular mechanisms of this phenomenon are not yet defined and require further research.

Inhibition of MEK/ERK/STAT3 signaling in oleuropein treatment inhibits myocardial ischemia/reperfusion

“…In AMI, long-term hypoxia and ischemia of myocardial cells leads to aerobic metabolic disorder due to coronary occlusion, and then causes hyperemia and edema of myocardial interstitial cells, and myocardial cell degeneration and necrosis, accompanied by a large amount of inflammatory cell infiltration (10). A large number of free radicals are generated in the tissues and the peroxide destruction of oxygen free radicals mainly damages the structure and function of myocardial cell membranes, damages the mitochondria, cuts off the cells energy supply and destroys lysosomes to cause cell autolysis (24). The myocardium of accelerated ischemia develops from reversible damage to irreversible degeneration and necrosis.…”

“…The myocardium of accelerated ischemia develops from reversible damage to irreversible degeneration and necrosis. Malignant arrhythmia appears, thereby causing ventricular remodeling and cardiac dysfunction (24). Recanalization and reperfusion therapy is the most effective treatment now, but I/R can further damage the myocardium, for which the important mechanism is oxidative stress; the greater the duration of myocardial ischemia and hypoxia the greater the oxidative stress and myocardial damage, and the more severe the disease (25).…”

Vitamin D Deficiency as It Relates to Oral Immunity and Chronic Periodontitis

“…The 1,25(OH) 2 D/VDR signalling pathway has the capacity to mediate antibacterial, antiviral, and anti-inflammatory activity [ 29 ]. VDR polymorphism has been associated with increased risk of several diseases, with some of the genetic variants being less responsive than others to 1,25(OH) 2 D in suppressing inflammatory processes, thus favouring the development of cutaneous inflammatory conditions [ 41 ] and possibly of chronic periodontitis [ 5 , 42 ].…”

“…In addition, it has been shown that VDR polymorphism, in the presence of exogenous aetiological factors (i.e., tobacco smoke and alcohol), is associated with increased risk of chronic periodontitis and other inflammatory conditions. Some genetic variants may be less responsive to 1,25(OH) 2 D in suppressing inflammation, thus favouring bacteria-induced tissue damage, while other variants are associated with low bone-mineral density, thus making alveolar bone vulnerable to bacterial plaque-induced inflammatory bone resorption [ 5 , 41 , 42 , 52 , 53 ].…”

Prevalence and Predictors of Low Serum 25-Hydroxyvitamin D among Female African-American Breast Cancer Survivors

“…Decreased cutaneous conversion of 7-dehydrocholesterol to cholecalciferol occurs with higher melanin content. 9 Accounting for skin pigmentation and sun behaviors are informative, yet understudied areas in the context of serum 25(OH)D and BC. Second, body mass index (BMI) has been used a surrogate marker of adiposity.…”