Effect of Nigella sativa L. and thymoquinone on rat platelet aggregation

The aim of the present study was to evaluate platelet responsiveness in rats following Nigella sativa L. [NS] and thymoquinone [TQ] administration. Additionally, the in vitro rat platelet aggregation response to TQ was investigated. Four doses of NS; 90, 180, 360 and 540 mg / Kg were fed daily to rats for 1, 2 and 4 weeks before running the aggregation study. TQ was administered as a single i. p. injection [4, 8, 12, 16 and; 20 mg /kg] 2-3 hours before testing the platelet response. Platelet rich plasma [PRP] was prepared from the treated rats, and platelet aggregation in response to collagen [10 micro,g / ml] and adenosine 5' - diphosphate [ADP; 20, 5 and 2.5 micro.M] was tested. Samples of 0.45 ml PRP from normal rats were also incubated with TQ [5, 10, 20, 50 micro.g] for 1 minute. Thereafter platelet aggregation response to collagen [10 micro g / ml] and ADP [20 micro.M] was performed by adding 0.05 ml of agonist [giving final concentrations of TQ 10, 20, 40, 100 micro,g / ml]. Platelet aggregation in response to collagen and ADP was not different in NS fed rats when compared with that in controls. Also tolerable doses of TQ [4 and 8 mg / Kg] and low concentration of TQ in vitro [10 micro.g / ml] neither affected collagen nor ADP induced platelet aggregation response. A dose of 12 mg TQ / Kg induced significant inhibition [p < 0.05] of platelet aggregation only when 2.5 micro.M of ADP was used for aggregation. Increasing TQ doses either in vivo or in vitro resulted in progressive inhibition of platelet aggregation. At a dose of 16 mg TQ / Kg there was significant inhibition by 25.1, 33.3, 74.7 and 75.7% with collagen and 20, 5 and 2.5 micro M ADP, respectively. The inhibition became more than 90% when 20 mg TQ / kg was administered. In vitro concentrations of TQ [20, 40 and 100 micro g / ml] caused significant inhibition of collagen and ADP [20 micro M]- induced aggregation by 37.8, 61.8,. 72% and 38.6, 83.1, 88.7%, respectively. These results suggest that regular consumption of NS would not influence platelet aggregation in humans. In the meantime, the findings show that TQ, NS major component, induces an inhibitory effect only when large doses are administered

Effect of selenium supplementation on plasma lipid and lipoprotein cholesterol levels in adult rats

Selenium is an antioxidant nutrient that prevents lipid peroxidation. The objective of the study was to investigate long-term effects of selenium supplementation on plasma lipid profile in rats. To investigate the effect of this micronutrient on plasma lipid levels, adult rats supplemented with selenium [20 micro g/Kg body weight] for 16 weeks were studied. Plasma selenium levels were found to be 167.9 +/- 4.8 micro g/1 and 193.9 +/- 3.8 micro.g/1 in control and selenium treated rats, respectively. Selenium supplementation significantly lowered the concentrations of plasma triglycerides by 21% and low density lipoprotein cholesterol [LDL-cho] by 42%. Also, the ratio of LDL-cho to either high density lipoprotein cholesterol [HDL-cho] or to total-cho was significantly lowered. On the other hand, selenium did not influence HDL-cho and total-cho concentrations although their relative ratio to each other was significantly increased [p<0.001]. Plasma selenium levels in the examined rats were negatively correlated with plasma triglycerides [r = -0.3479] and LDL-cho [r = -0.3177] concentrations. Therefore, the food supplementation with selenium might be beneficial in improving lipid profile, the major risk factor for coronary heart disease [CHD]

Royal jelly, a possible agent to reduce the nicotine-induced atherogenic lipoprotein profile

The study investigated the effect of royal jelly on the nicotine-induced atherogenic lipoprotein profile. To evaluate the changes in lipid and lipoprotein cholesterol concentrations, royal jelly [1 mg/g body weight/day] and/or nicotine [0.05 mg/ml in drinking water, a dose which simulated intake by heavy smokers] were tested in adult male rats, following 8 weeks of their oral supplementation. Neither royal jelly nor nicotine or their combination significantly changed serum total cholesterol and triglyceride levels. Additionally royal jelly did not significantly change serum lipoprotein cholesterol concentrations. Oral nicotine alone progressively inhibited weight gain and significantly lowered the high density lipoprotein cholesterol level and its ratio to the total cholesterol [by 19% and 23% respectively]. Also nicotine elevated the low density lipoprotein/high density lipoprotein [LDL/HDL] cholesterol ratio [82%] significantly. On the other hand, royal jelly when given to nicotine treated rats increased the HDL cholesterol and HDL/total cholesterol ratio and decreased the LDL/HDL cholesterol ratio to reach values insignificantly different from the control. Royal jelly also prevented the progressive decline in body weight gain caused by nicotine administration. Our data demonstrated that royal jelly is a potential antiatherosclerotic agent capable of improving the nicotine-induced atherogenic lipoprotein profile