1. The present study was undertaken to compare the effects of a higher dose of policosanol, a cholesterol-lowering drug, (40 mg/day) with the effects of 20 mg/day policosanol on platelet aggregation in healthy volunteers and type II hypercholesterolaemic patients. 2. Study subjects were randomized to receive, under double-blind conditions, placebo or policosanol (20 or 40 mg/day) for 30 days once a day. Blood sampling was performed at baseline and after 30 days on therapy. 3. Platelet aggregation was induced with three aggregating agents: arachidonic acid (AA), collagen and low doses of ADP. 4. Policosanol (20 and 40 mg/day) moderately yet significantly reduced platelet aggregation, but no differences were observed in the effects produced by either dose of policosanol. In healthy volunteers, policosanol at 20 and 40 mg/day inhibited aggregation induced by 2 mmol/L AA (28.2 and 24.9%, respectively), 1 micro g/mL collagen (21.1 and 20.2%) and 1 micro mol/L ADP (30.9 and 29.1%). Changes that occurred following the administration of placebo were not significant, although an upward trend for collagen- and ADP-induced aggregation occurred in normal and hypercholesterolaemic subjects, respectively, thus partially masking the effects of policosanol on these responses. 5. The antiplatelet effects of policosanol at 20 and 40 mg/day in hypercholesterolaemic patients were also similar, so that both doses inhibited aggregation induced by 1.5 mmol/L AA (20.1 and 33.0%, respectively), 0.5 micro g/mL collagen (22.7 and 21.1%) and 1 micro mol/L ADP (40.5 and 34.7%). 6. In addition, after 30 days of therapy, 20 and 40 mg/day policosanol significantly (P < 0.01) reduced low-density lipoprotein-cholesterol (15.9 and 17.0%, respectively) and total cholesterol (12.4 and 12.3%, respectively; P < 0.05), yet increased high-density lipoprotein-cholesterol values by 5% in both groups (P < 0.05). 7. Triglycerides were decreased compared with baseline, but not with respect to the placebo. 8. We conclude that the antiplatelet effects induced by 40 mg/day policosanol administered for 30 days to healthy volunteers and to hypercholesterolaemic patients were similar to the effects induced by 20 mg/day policosanol. Thus, no enhancement of the response was achieved with the use of a higher dose of policosanol in study patients.

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Policosanol is a mixture of higher aliphatic alcohols purified from sugar cane wax, with cholesterol-lowering effects demonstrable in experimental models and in patients with type II hypercholesterolemia. The protective effects of policosanol on atherosclerotic lesions experimentally induced by lipofundin in rabbits and rats and spontaneously developed in stumptail monkeys have been described. The present study was conducted to determine whether policosanol administered orally to rabbits with exogenous hypercholesterolemia also protects against the development of atherosclerotic lesions. Male New Zealand rabbits weighing 1.5 to 2 kg were randomly divided into three experimental groups which received 25 or 200 mg/kg policosanol (N = 7) orally for 60 days with acacia gum as vehicle or acacia gum alone (control group, N = 9). All animals received a cholesterol-rich diet (0.5%) during the entire period. Control animals developed marked hypercholesterolemia, macroscopic lesions and arterial intimal thickening. Intima thickness was significantly less (32.5 ± 7 and 25.4 ± 4) in hypercholesterolemic rabbits treated with policosanol than in controls (57.6 ± 9). In most policosanol-treated animals, atherosclerotic lesions were not present, and in others, thickness of fatty streaks had less foam cell layers than in controls. We conclude that policosanol has a protective effect on the atherosclerotic lesions occurring in this experimental model.

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D-002 is an anti-ulcerogenic product, isolated from beeswax, which consists of a well-defined mixture of higher primary aliphatic alcohols. It is highly effective against ethanol-induced ulcers. This study was designed to determine if D-002 shows cytoprotective properties on gastric mucosa in ethanol-induced ulcers. The involvement of endogenous prostaglandins in the protective effect of D-002 was also investigated. When a subulcerogenic dose of indomethacin (10 mg kg-1) was injected simultaneously with oral administration of ethanol, oral pre-treatment with D-002 (5-100 mg kg-1) partially inhibited the gastric protection. D-002 (5 and 25 mg kg-1) administered to normal rats significantly increased the soluble mucus content and also prevented its reduction in rats with ethanol-induced ulcers. In addition, D-002 administered at 5 and 25 mg kg-1 prevented the increase of vascular permeability induced by ethanol (60%) and reduced the concentration of thromboxane B2 (TXB2) in gastric mucosa of rats with ethanol-induced ulcers. These results support the hypothesis that the anti-ulcerogenic properties of D-002 could be related to a cytoprotective mechanism.

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