Fibrinogen facilitates atherosclerotic formation in Sprague-Dawley rats: A rodent model of atherosclerosis

Fibrinogen (Fg) contributes to thrombosis and hemostasis and plays a role in inflammation. Fg is also known to play a significant role in atherosclerosis (AS). P-selectin has been associated with AS. The present study aimed to identify the role of Fg in AS and to examine the possible mechanisms behind the effects of fibrinogen on AS using Sprague-Dawley (SD) rats as a model system. Diet-induced atherosclerotic SD rats were adopted as the experimental models. Fg was transfused into these rats and the degree of atherosclerotic lesion development was compared with that of control rats. Blood was obtained from the common abdominal aorta and then the biochemical characteristics were measured and ELISA assays performed. The aortas were then carefully separated, removed and placed in 10% (w/v) neutral formalin for use at a later stage. The root of the aorta was cut and samples were washed, dehydrated, cleared, dipped in wax, embedded, sliced, coated, grilled and stained with HE. Pathological HE-stained sections were examined by light microscopic analysis and immunohistochemistry was performed for Fg and P-selectin on representative tissue sections. The Fg-transfused, high-fat diet-fed group developed atherosclerotic lesions more readily compared with the control group. Immunohistochemical analysis revealed that Fg expression was higher in the endarterium of the Fg-transfused, high-fat diet-fed rats. P-selectin expression was also found to be correlated with Fg expression. Fg actively promotes atherosclerotic lesion development; one possible mechanism behind this is the ability of Fg to enhance P-selectin expression, which is also able to facilitate the development of atherosclerotic lesions.