The Journal of Japan Atherosclerosis Society
Online ISSN : 2185-8284
Print ISSN : 0386-2682
ISSN-L : 0386-2682
Effects of Elastase on Plasma and Aortic Lipoproteins in Cholesterol-fed Rabbits
Tomio KAMETANI
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1978 Volume 6 Issue 1 Pages 101-113

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Abstract

Effects of elastase on plasma and aortic lipoproteins in 1% cholesterol-fed rabbits were investigated.
Elastase was injected (4mg/rabbit/day) i.m. in 8 cholesterol-fed rabbits for 12 weeks.
Marked hypercholesterolemia and atherosclerosis were produced by cholesterol-feeding. In the cholesterol-fed rabbits, cholesterol-rich VLDL and apoprotein R-2 and 3 of VLDL, which are called as arginine-rich apoproteins, increased.
The plasma cholesterol, VLDL-cholesterol and VLDL-apoproteins were significantly lower in the elastase-treated rabbits than in the cholesterolfed rabbits (P<0.05, P<0.02, P<0.01). The plasma triglyceride and LDL-cholesterol levels were lower in the elastase-treated rabbits (not significant). The lower plasma cholesterol level in the elastase-treated rabbits was produced through the decrease of VLDL-cholesterol level.
Some authors report that elastase increases the catabolism of cholesterol in liver and the excretion of bile acids. Therefore, the present data suggest that elastase decreases plasma cholesterol and VLDL-cholesterol through the increase of uptake and catabolism of VLDL “remnant” in liver.
Both VLDL- and LDL-cholesterol contents, particularily LDL-cholesterol, in the aortic intima and media increased significantly in the cholesterol-fed rabbits.
Macroscopicaly, elastase tended to inhibit the atherosclerosis of aorta. Elastase decreased the VLDL- and LDL-cholesterol contents of the aorta, although statistically insignificant. Since LDL has more atherogenecity than VLDL, elastase might not have shown a significant antiatherogenecity. While there was no difference in plasma LDL-cholesterol between the cholesterol-fed and the elastase-treated rabbits, the aortic LDL-cholesterol content in the latter were almost half that in the former. Thus, elastase was thought to have directly inhibited the deposition of LDL in the arterial wall.

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