## 5 Discussion
The latter compound, identified as erucamide (13-docosenamide), is known to act on the central nervous system, and it may promote angiogenesis; it also has anti-cancer and antimicrobial properties [37]. According to the study of [PERSON] et al., this compound might be produced by the host-bacteria interaction when glucose is present [38]. We hypothesize that rivaroxaban may also influence the metabolism of HUVEC cells and may alter it. It has been determined that erucamide production is lower in samples in the presence of higher rather than lower rivaroxaban concentrations. Future research is required for a better understanding of the correlation between erucamide production and rivaroxaban concentrations. This study also evaluated changes in the mRNA level and the concentrations of the cytochrome P450 family enzyme CYP4F2, known as \(\omega\)-hydroxylase, in HUVECs induced by treatment with different concentrations of rivaroxaban. [PERSON] et al., who studied the effect of rivaroxaban on HUVECs, had determined that rivaroxaban, in a concentration-dependent manner, increases cell viability, growth and migration via the urokinase plasminogen activator by inducing its expression [39]. The team also determined that rivaroxaban neutralizes the FXa-induced expression of inflammatory genes and platelet adhesion in HUVECs. These results demonstrate the ability of rivaroxaban to improve endothelial function in CVD. It is known that rivaroxaban exhibits anti-inflammatory properties. The exposure of HUVECs to rivaroxaban resulted in a significant concentration-dependent downregulation of inflammatory genes _VCAM-1, ICAM-1_ and _IL-8_[40]. Another study investigating the effects of oxidized cholesterol on HUVECs showed that rivaroxaban may reduce elevated ROS levels in cells [41]. ROS is involved in inflammatory processes and induces the development of atherosclerosis. The results of our study demonstrated the potential antioxidant properties and benefits of rivaroxaban in the prevention of atherosclerosis. The amount of CYP4F2 enzyme is found to be optimal 24 h after the onset of inflammation [42, 43, 44]. In our study, after treatment with different doses of rivaroxaban (0.1, 0.2, 0.5, 1, 2, 5 and 10 uM), the expression of the CYP4F2 gene in HUVECs was downregulated by 1.44-, 1.71-, 1.89-, 1.93-, 2.05-, 2.4- and 2.72-fold in a concentration-dependent manner compared to control cells. The downregulation of _CYP4F2_ expression decreases the amount of gene transcript and the rate of \(\omega\)-hydroxylase synthesis of its encoded protein. \(\omega\)-hydroxylase is one of the major enzymes in the CYP family involved in the metabolism of arachidonic acid to form biologically active eicosanoids, such as 20-HETE. CYP4F2 also metabolizes leukotriene B4 (LTB4), which is formed/synthesized during the development of inflammation [42, 43, 44]. No other studies have been performed to evaluate the effect of rivaroxaban on the enzyme \(\omega\)-hydroxylase in endothelial cells. The effect of hsa-miR-24-3p on target genes was further evaluated in this study. A potential hsa-miR-24-3p gene target, _HNF4a_, was selected for this study after a detailed analysis of information found on miRNA target databases (TargetScan v.7.2, miRTarBase 7.0) and PubMed. [PERSON] et al. were the first to describe the regulation of _HNF4a_ by miR-24 in vitro [45]. The potential recognition elements of miR-24 were identified in _HNF4a_ coding and the 3' UTR region. The study showed that miR-24 also reduced the expression of various gene targets, including cytochrome P450 7A1 and 8B1 isoforms, by inhibiting _HNF4a_ expression. The fact that miR-24-3p acts as an effector molecule of _HNF4a_ and indirectly contributes to the regulation of other genes has also been confirmed by the [PERSON] study [46]. After the analysis of the previously mentioned miRNA databases, it was determined that the 3' UTR region of _CYP4F2_ lacks hsa-miR-24-3p binding sites.