Intake of Korean red ginseng (KRG, ginseng Radix rubra), rich in glycosylated saponins (ginsenosides), has been known to inhibit platelet aggregation in the normocholesterolemic condition. However, it is unclear whether KRG can attenuate hypercholesterolemia-enhanced platelet aggregation. This study examined whether the daily consumption of a KRG-water extract (WE) could prevent the hypercholesterolemia-enhanced platelet aggregation and progression of hypercholesterolemic atherosclerosis. KRG-WE administration (200 mg/kg/day) for 8 weeks potently inhibited the platelet aggregation induced by low doses of agonists (0.5 microg/mL collagen and 0.025 unit/mL thrombin), whereas it weakly reduced the blood-cholesterol levels and formation of atheromatous lesions. In further investigation, KRG-WE significantly suppressed collagen-induced 1,2-diacylglycerol liberation, but had no significant effect on arachidonic acid liberation. Taken together, it can be suggested that the antiplatelet effect of KRG-WE may, at least partly, be due to the inhibition of 1,2-diacylglycerol generation rather than regulation of blood lipid levels. In conclusion, daily consumption of KRG-WE could be a useful alternative measure for the prevention of thrombus and atheroma formation in hypercholesterolemia.

OBJECTIVES To determine the detrimental role of tetrachlorodibenzo‐p‐dioxin (TCDD) in testicular histology, spermatogenesis‐related panels and proteome, and serum sex hormone levels. MATERIALS AND METHODS In all, 40 male rats were divided into equal groups: a normal control (NC) group that received vehicle and saline, and a TCDD‐treated (TT) group injected intraperitoneally with TCDD (one dose, 50 µg/kg body weight). The rats were killed 4 weeks after TCDD exposure and testicular weight, histopathology, proteome and variables related to spermatogenesis, and serum sex hormone levels were investigated. RESULTS TCDD induced a significant decrease in testicular weight, Johnsen’s score, seminiferous tubular size, percentage of tubules containing sperm, sperm counts, germ cell counts and Sertoli cell index. In addition, there was a significant decrease in serum testosterone level (P < 0.01) and a remarkable increase in oestradiol (P < 0.01), follicle‐stimulating hormone (P < 0.05) and luteinizing hormone (P < 0.05) levels in the TT group. The expression of six testicular proteins including testis‐specific heat shock protein (Hsp70), protein disulphide isomerase A3 precursor, 3‐phosphoglycerate dehydrogenase, nonmuscle myosin heavy‐chain type B‐like protein, and superoxide dismutase 1 were significantly up‐regulated (P < 0.05–0.01). Interestingly, fertility protein SP22 and phosphatidylethanolamine‐binding protein were down‐regulated but this was only significant for fertility protein SP22 (P < 0.05). CONCLUSION TCDD induces marked histological changes in the testis, impairs variables related to spermatogenesis, and increases serum oestradiol levels but decreases testosterone levels. In particular, TCDD disturbs testicular proteome profiles in rats.