Preliminary observation of regressive effect of atorvastatin on aorta atherosclerosis in rabbits
Zhu Yan
Abstract
Zhu Yan
Abstract
[Objective] To determine the effect of atorvastatin on aorta expression of plasminogen activator inhibitor type1-1(PAI-1)and it/s mechanism of anti-atherosclerosis in atheroclerosis rabbits fed with cholesterol-enriched diet. [Methods] Twenty four rabbits were randomly divided into control, cholesterol diet and atorvastatin group, which were fed for 16 weeks. Serum TC, LDL and weigh were measured in 0 and 16 weeks in the three groups. The aortas were harvested for pathologic morphology observation, immunohistochemistry analysis of PAI-1 positive percentages was performed. [Results] After 16 weeks TC and LDL in atorvastatn group were greatly lower than that cholesterol diet group (P 0.01), they were (23.51±10.58) mmol/L and (14.27±3.51) mmol/L(P 0.01), (21.39±10.00) mmol/L vs (14.23±4.01) mmol/L (P 0.01). The aortas plaque/intima size (P/I) was 0, (0.28±0.37) vs (0.16±0.27) in control, cholesterol diet group and atorvastatn group by pathologic nakey observation(P 0.01), intima thickness was (4.45±0.58) μm, (67.47±7.13) μm and (38.11±6.02) μm, intima/medium thickness ratio(I/M) was (0.0537±0.007), (0.878±0.370) and (0.391±0.213) in the three groups by microscope(P 0.01). The expressions of immunohistochemistry analysis of PAI-1 in cholesterol diet group and atorvastatin group were higher than that control(P 0.01), but the expression reduced in atorvastatin group (P 0.01). [Conclusion] Atorvastatin has anti-atherosclerosis effect except reducing serum lipids, the inhibition of PAI-1 excessively expression may be one of the anti-atherosclerosis mechanism.
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[Objective] To determine the effect of atorvastatin on aorta expression of plasminogen activator inhibitor type1-1(PAI-1)and it/s mechanism of anti-atherosclerosis in atheroclerosis rabbits fed with cholesterol-enriched diet. [Methods] Twenty four rabbits were randomly divided into control, cholesterol diet and atorvastatin group, which were fed for 16 weeks. Serum TC, LDL and weigh were measured in 0 and 16 weeks in the three groups. The aortas were harvested for pathologic morphology observation, immunohistochemistry analysis of PAI-1 positive percentages was performed. [Results] After 16 weeks TC and LDL in atorvastatn group were greatly lower than that cholesterol diet group (P 0.01), they were (23.51±10.58) mmol/L and (14.27±3.51) mmol/L(P 0.01), (21.39±10.00) mmol/L vs (14.23±4.01) mmol/L (P 0.01). The aortas plaque/intima size (P/I) was 0, (0.28±0.37) vs (0.16±0.27) in control, cholesterol diet group and atorvastatn group by pathologic nakey observation(P 0.01), intima thickness was (4.45±0.58) μm, (67.47±7.13) μm and (38.11±6.02) μm, intima/medium thickness ratio(I/M) was (0.0537±0.007), (0.878±0.370) and (0.391±0.213) in the three groups by microscope(P 0.01). The expressions of immunohistochemistry analysis of PAI-1 in cholesterol diet group and atorvastatin group were higher than that control(P 0.01), but the expression reduced in atorvastatin group (P 0.01). [Conclusion] Atorvastatin has anti-atherosclerosis effect except reducing serum lipids, the inhibition of PAI-1 excessively expression may be one of the anti-atherosclerosis mechanism.
Key concepts: Atorvastatin, Aorta, Internal medicine, Cholesterol, Immunohistochemistry, Endocrinology, Medicine, Arteriosclerosis