ABSTRACT
Objective: To observe the changes of endothelial-dependent vasodilatation and cyclophilin A (CyPA) expression at different phases of atherosclerosis in experimental rats. Methods: A total of 30 male Wistar rats were divided into 4 groups: Control group, the rats received normal diet, and 3 atherosclerosis groups, the rats received high cholesterol diet for different period of time and a single dose intraperitoneal injection of Vitamin D3 at 600,000 IU/kg, as Atherosclerosis at 8 weeks (AS 8W) group, AS 12W group and AS 15W group, n=8 in each AS group. The rats were sacriifced at the same time to isolate aorta abdominalis. The expression of CyPA at the wall of aorta abdominalis was detected by HE staining and immunohistochemistry. In addition, the aorta abdominalises was cut into 5 mm rings to observe its response to acethylcholine in exvivo organ bath. Results: With prolonged modeling time, the rats at different groups presented normal vessel structure, endothelial cell damage, vessel smooth muscle cell proliferation, atherosclerosis plaque formation and calciifed plaque formation for differentpathological characteristics. The endothelial-dependent vasodilatation was decreased and the maximum vasodilatation percentage in Control group, AS 8W group, AS 12W group and AS 15W group were at (93.46 ± 2.80) %, (82.58 ± 3.25) %, (61.19 ± 3.72)% and (41.28 ± 2.68)% respectively,P<0.05 between each group. The CyPA expression in endothelial cell and vessel smooth muscle cell were increased accordingly in 4 groups by OD value as (0.25 ± 0.06), (0.34 ± 0.09), (0.53 ± 0.09) and (0.68 ± 0.13) respectively,P<0.05 between each group. Conclusion: The CyPA expression increased and the endothelial-dependent vasodilatation decreased with the progress of atherosclerosis accordingly in experimental rats. The expression level of CyPA is related to atherosclerosis degree and it is one of the initial factors for atherosclerosis in rats.
ABSTRACT
Under pathological conditions,promoting oxidative stress kinase to be activated in the body,mitochondrial respiratory chain abnormalities,and decreased oxygen free radical scavenging capacity lead to increased oxygen free radicals and pro-oxidant factors.The accunulation of the above harmful substances lead to the corresponding changes of arterial wall and blood components,such as endothelium-dependent relaxation dysfunction,inflammatory cytokine activation,endothelial structural damage,vascular smooth muscle cell proliferation,and foam cell formation,thus play key roles in the processes of the occurrence and development of atherosclerosis.The role of antioxidant therapy in the prevention of cardio-cerebrovascular events remains controversial and needs to be further studied.