2006•Unpublished venueRequires access

The Mechanism of the Anti-atherosclerosis Effect by Atorvastatin

Lei Yu

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Abstract

ObjectiveTo study the effect of atorvastatin on aorta atherosclerosis in rabbits and explore the possible mechanism.MethodsTwenty four rabbits were randomly divided into control, cholesterol fed, and atorvastatin treated group.Serum TC, TG, LDL, VCAM-1, PAI-1 and weight were measured at 0 and 16 weeks.After 16 weeks, the aortas were harvested for pathologic morphology study. Immunohistochemistry analysis was used for evaluating the positive rates of VCAM-1 and PAI-1.Results There were no differences in TC, TG, LDL, VCAM-1 and PAI-1 in three groups in 0 week(P0.05).After 16 weeks TC, LDL, VCAM-1 and PAI-1 in cholesterol fed group and atorvastatn group were signifcantly greater than that in control group, while TC, LDL, VCAM-1 and PAI-1 in atorvastatn group greatly lower than cholesterol diet group(P0.01).The aortas plaque/intima size(P/I) ratio were 0, 0.281±0.037 and 0.161±0.027 in control, cholesterol diet group and atorvastatn group, respectively (P0.01). Intima thickness was 4.45±0.58, 67.47±7.13 and 38.11±6.02 μm along with intima/medium thickness ratio(I/M) of 0.054±0.007, 0.878±0.370 and 0.391±0.213 in the three groups(P0.01).The expressions of immunohistochemistry analysis of VCAM-1 and PAI-1 in aorta in cholesterol fed and atorvastatin group were greater than that in control(P0.01), which was again reduced in atorvastatin group(P0.01).ConclusionAtorvastatin inhibits the excessively expressions of VCAM-1 and PAI-1 in aortic atherosclerosis leison which is likely to be one of its antiatherosclerocis mechanism.

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ObjectiveTo study the effect of atorvastatin on aorta atherosclerosis in rabbits and explore the possible mechanism.MethodsTwenty four rabbits were randomly divided into control, cholesterol fed, and atorvastatin treated group.Serum TC, TG, LDL, VCAM-1, PAI-1 and weight were measured at 0 and 16 weeks.After 16 weeks, the aortas were harvested for pathologic morphology study. Immunohistochemistry analysis was used for evaluating the positive rates of VCAM-1 and PAI-1.Results There were no differences in TC, TG, LDL, VCAM-1 and PAI-1 in three groups in 0 week(P0.05).After 16 weeks TC, LDL, VCAM-1 and PAI-1 in cholesterol fed group and atorvastatn group were signifcantly greater than that in control group, while TC, LDL, VCAM-1 and PAI-1 in atorvastatn group greatly lower than cholesterol diet group(P0.01).The aortas plaque/intima size(P/I) ratio were 0, 0.281±0.037 and 0.161±0.027 in control, cholesterol diet group and atorvastatn group, respectively (P0.01). Intima thickness was 4.45±0.58, 67.47±7.13 and 38.11±6.02 μm along with intima/medium thickness ratio(I/M) of 0.054±0.007, 0.878±0.370 and 0.391±0.213 in the three groups(P0.01).The expressions of immunohistochemistry analysis of VCAM-1 and PAI-1 in aorta in cholesterol fed and atorvastatin group were greater than that in control(P0.01), which was again reduced in atorvastatin group(P0.01).ConclusionAtorvastatin inhibits the excessively expressions of VCAM-1 and PAI-1 in aortic atherosclerosis leison which is likely to be one of its antiatherosclerocis mechanism.

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Available abstract

ObjectiveTo study the effect of atorvastatin on aorta atherosclerosis in rabbits and explore the possible mechanism.MethodsTwenty four rabbits were randomly divided into control, cholesterol fed, and atorvastatin treated group.Serum TC, TG, LDL, VCAM-1, PAI-1 and weight were measured at 0 and 16 weeks.After 16 weeks, the aortas were harvested for pathologic morphology study. Immunohistochemistry analysis was used for evaluating the positive rates of VCAM-1 and PAI-1.Results There were no differences in TC, TG, LDL, VCAM-1 and PAI-1 in three groups in 0 week(P0.05).After 16 weeks TC, LDL, VCAM-1 and PAI-1 in cholesterol fed group and atorvastatn group were signifcantly greater than that in control group, while TC, LDL, VCAM-1 and PAI-1 in atorvastatn group greatly lower than cholesterol diet group(P0.01).The aortas plaque/intima size(P/I) ratio were 0, 0.281±0.037 and 0.161±0.027 in control, cholesterol diet group and atorvastatn group, respectively (P0.01). Intima thickness was 4.45±0.58, 67.47±7.13 and 38.11±6.02 μm along with intima/medium thickness ratio(I/M) of 0.054±0.007, 0.878±0.370 and 0.391±0.213 in the three groups(P0.01).The expressions of immunohistochemistry analysis of VCAM-1 and PAI-1 in aorta in cholesterol fed and atorvastatin group were greater than that in control(P0.01), which was again reduced in atorvastatin group(P0.01).ConclusionAtorvastatin inhibits the excessively expressions of VCAM-1 and PAI-1 in aortic atherosclerosis leison which is likely to be one of its antiatherosclerocis mechanism.

Key concepts: Atorvastatin, Internal medicine, Aorta, Cholesterol, Endocrinology, Immunohistochemistry, Medicine, Arteriosclerosis

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