The results obtained from this study indicate that in high cholesterol diets, cornus mas L. and lovastatin can reduce the fibrinogen level.
Fibrinogen is an inflammatory and coagulation risk factor and has an important role in the complexity of atherosclerosis process.16
The enforcement of platelet aggregation and formation of fibrin coagulum are among the primary functions of fibrinogen during homeostasis process in the arterial injury site.17
It has been reported that fibrinogen oxidation and its fibrinolyze residuals stimulate platelet aggregation and IL-6 increment,16
and therefore the reducing effects of cornus mas L. on fibrinogen levels can be due to the participation of its components in inflammatory or coagulative processes.
There have been studies showing the effects of herbal diets on the processes of inflammation and fibrinolyze. These compounds are effective in the reduction of coagulative factors, or the augmentation of fibrinolyze via reducing blood coagulation by means of decreasing fibrinogen levels, increasing fibrinolyze and prothrombin time, and also preventing platelet aggregation.18
The anti-inflammatory and arterial protective effects20
of anthocyanins, which are among the most important antioxidants in cornus mas L. fruit,21
along with their usefulness in the excretion of free radicals, have been investigated.8
Research shows that the consumption of antioxidants will increase the antioxidantal capacity and decrease cardiovascular disease development chance, and also the risk associated with raised fibrinogen level.25
As a result, it is probably true that the antioxidant compounds in cornus mas L. fruit, including vitamins and phenolic compounds, would prevent free radical action and fibrinogen oxidation and its fibrinolyze residuals, which stimulate platelet aggregation and increase inflammatory cytokines.
Inflammation and platelet aggregation will increase fibrinogen production in the liver by 4 times. On the other hand, Fibrinogen level increases in response to interleukins 1 and 6 (cytokines produced in arterial disorders).26
Evidence suggests that the bare matrix under an injured endothelium contains a great amount of pre-coagulation compounds, including collagen. In the process of absorption and activation of platelets, collagen acts like a ligand. In other words, just like a strong antagonist, collagen causes the release of platelet granules and the presentation of active ligands, such as IIb- IIIa. Platelet granules contain VWF (Von Willebrand Factor) and fibrinogen which act as a connecting bridge between the collagen under endothelium and glycoprotein platelet receptor (GPTb). The process of platelet aggregation continues as fibrinogen connects a big number of platelets to each other via GPIIb-IIIa platelet receptors.27
Research shows that in the inflammation and arterial wall injury site, anthocyanins and anthocyanidins affect the structure and metabolism of collagen and cause stronger collagen fibers and better crosslink among them (via affecting proline hydroxylase enzyme), and actually prevent collagens from attaching to platelets in the primary stages of inflammation and arterial injury.28
In addition, anthocyanic extract stops inflammation, and thus atherosclerosis progress, by preventing elastase enzyme (a collagen destructive enzyme) from action.29
It has been observed that polyphenols existing in cocoa reduce the inflammatory cytokinines and inhibit platelet activity and epinephrine gene (a platelet aggregation agonist that is produced at platelet aggregation site) expression and also glycoprotein IIa/IIIbv on the platelet surface; in addition, they reduce P-Selection expression (as an inflammatory agent).30
Research shows that delphinidin and pelargonin glycosides, existing in cornus mas L. fruit, inhibit cyclooxygenase inflammatory enzymes activity31
and therefore reduce the levels of pre-inflammatory compounds and cytokinines. Recent studies have demonstrated that polyphenols such as catechin and quercetin, stop NADPH oxidase enzyme (existing in platelets), thus inhibiting the production of O2-
and increasing the biological power of NO, and consequently regulate the glycoprotein pine receptors on platelet membrane surface (GPIIb-IIIa) which in turn inhibits the platelets activation and their adherence during the inflammation and thrombosis processes 33
Consumption of lovastatin has also led to a reduction in fibrinogen level compared to the high cholesterol group.
Statins are a group of antihyperlipidemic compounds and anti-inflammatory effects are amongst their most important pleiotropic qualities. These effects are due to the ability of statins in preventing mevolonic acid formation, whose reduction results in a decrease in cholesterol level and some other isoprenoid inflammatory mediators.34
It was also observed that in hyperlipidemic patients, statins reduce the platelet adhesive molecules, ICAM-1 and P-Selection; they also decrease MCP-1 expression, interleukins 1 and 6 production, and oxygenase-2 cycle gene expression in human endothelial cells.35
In fact, statins reduce platelet clot and cardiovascular diseases via decreasing inflammatory agents and affecting homeostase process and NO production by endothelial cells.38