Effects of probucol on homozygous cases of familial hypercholesterolemia

Yamamoto, Akira; Matsuzawa, Yūji; Kishino, B; Hayashi, Rikuro; Hirobe, Kazuhiko; Kikkawa, T

doi:10.1016/0021-9150(83)90102-8

Cited by 105 publications

(23 citation statements)

References 15 publications

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“…Quinn et al have reported that oxidized LDL has inhibitory effect on the endothelial cell-derived chemotactic activity for mouse peritoneal macrophages (39). In addition, Parthasarathy et al (40) have also reported that probucol, a known inhibitor ofboth progression of atherosclerotic lesion and xanthoma formation (41) In our study we have demonstrated that major stimulatory activity on arachidonate metabolism exists in the lipoproteinlipid peroxide complex, and not in free lipid peroxides (Fig. 8).…”

Section: Discussionsupporting

confidence: 65%

Stimulated arachidonate metabolism during foam cell transformation of mouse peritoneal macrophages with oxidized low density lipoprotein.

Yokode¹,

Kita²,

Kikawa³

et al. 1988

J. Clin. Invest.

155

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Changes in arachidonate metabolism were examined in mouse peritoneal macrophages incubated with tarious types of lipoproteins. Oxidized low density lipoprotein (LDL) was incorporated by macrophages and stimulated macrophage prostaglandin E2 (PGE2) and leukotriene C4 syntheses, respectively, 10.8-and 10.7-fold higher than by the control. Production of 6-keto-PGFI,, a stable metabolite of prostacyclin, was also stimulated. No stimulation was found with native LDI, which was minimally incorporated by the cells. Acetylated LDL and beta-migrating very low density lipoprotein (Ol-VLDL), though incorporated more efficiently than oxidized LDL, also had no stimulatory effect. When oxidized LDL was separated into the lipoprotein-lipid peroxide complex and free lipid peroxides, most of the stimulatory activity was found in the former fraction, indicating that stimulation of arachidonate metabolism in the cell is associated with uptake of the lipoprotein-lipid peroxide complex. These results suggest that peroxidative modification of LDL could contribute to the progression of atheroma by stimulating arachidonate metabolism during incorporation into macrophages.

show abstract

Section: Discussionsupporting

confidence: 65%

Stimulated arachidonate metabolism during foam cell transformation of mouse peritoneal macrophages with oxidized low density lipoprotein.

Yokode¹,

Kita²,

Kikawa³

et al. 1988

J. Clin. Invest.

155

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“…Probucol treatment has been shown to reduce LDL and high density lipoprotein cholesterol levels in humans 20 and to have similar effects in rabbits.…”

Section: Discussionmentioning

confidence: 98%

“…Probucol-treated animals had higher triglyceride levels and lower high density lipoprotein levels than did controls; this is an expected effect of probucol treatment. 12 -13 - 20 Although total cholesterol levels were not different between groups, probucol treatment was associated with a marked decrease (as compared with controls) in the amount of atheroscle- rosis present, as judged by the mean percentage of thoracic aortic surface area involved with plaque. Total thoracic aortic surface area involved with plaque for probucol-treated animals was 23.0±12.5% (mean±SD, n=6) and for control animals was 81.2±20.4% (n=6; not determined for one animal).…”

Section: Plasma Lipids and Lipoproteins And Atherosclerotic Involvemementioning

confidence: 93%

Probucol treatment affects the cellular composition but not anti-oxidized low density lipoprotein immunoreactivity of plaques from Watanabe heritable hyperlipidemic rabbits.

O’Brien

Nagano

Gown

et al. 1991

Arterioscler Thromb

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“…5 " 7 For homozygotes, however, oral drugs have little effect on plasma LDL levels, with the exception of probucol, which has some effect. 8 Therefore, direct removal of LDL from the patients' plasma by plasmapheresis is the best treatment for homozygotes and for those heterozygotes for whom oral drugs are not effective.…”

mentioning

confidence: 99%

Selective removal of low density lipoprotein by plasmapheresis in familial hypercholesterolemia.

Yokoyama¹,

Hayashi²,

Satani³

et al. 1985

Arteriosclerosis

241

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Plasma lipoproteins were selectively removed from familial hypercholesterolemic patients by using two types of plasmapheresis: double-membrane filtration and selective adsorption of very low density lipoproteins (VLDL) and low density lipoproteins (LDL). In both techniques, plasma was separated from blood cells by using hollowfiber filters, and 100% of the VLDL and LDL was recovered in the filtrate. In doublemembrane filtration, the second hollow-fiber filter trapped 84% of LDL + VLDL, 48% of high density lipoprotein ( P lasma low density lipoprotein (LDL) has been recognized as a primary risk factor for developing atherosclerotic vascular lesions, especially in coronary arteries.1 Reduction of the plasma LDL level has been shown to decrease the incidence of ischemic heart attack in hyperlipoproteinemic patients. 2On the other hand, the plasma high density lipoprotein (HDL) level is inversely correlated, in epidemiological studies, 3 to the incidence of coronary heart disease independently of plasma LDL contribution. Thus, the risk of coronary heart disease must be considered from both of these aspects.

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Effects of probucol on homozygous cases of familial hypercholesterolemia

Cited by 105 publications

References 15 publications

Stimulated arachidonate metabolism during foam cell transformation of mouse peritoneal macrophages with oxidized low density lipoprotein.

Stimulated arachidonate metabolism during foam cell transformation of mouse peritoneal macrophages with oxidized low density lipoprotein.

Probucol treatment affects the cellular composition but not anti-oxidized low density lipoprotein immunoreactivity of plaques from Watanabe heritable hyperlipidemic rabbits.

Selective removal of low density lipoprotein by plasmapheresis in familial hypercholesterolemia.

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