Hypolipidemic and hypocholesterolemic effect of argan oil (Argania spinosa L.) in Meriones shawi rats.

The potential health benefits of various dietary oils in relation to cardiovascular disease and cancer are recently receiving considerable attention. The main proposal of this study is to investigate the effect of dietary argan oil, obtained from seeds of Argania spinosa L. (Sapotaceae) endemic from Morocco, on serum lipids composition. Hyperlipidemia was induced by high calorie and cholesterol (HCC) diet administration in 16 rats (Meriones shawi, a rodent of the Gerbillideae family). Eight rats were treated with argan oil (1ml/100g weight) daily by oral route during 7 weeks (treated group). Control animals were also fed with HCC diet for 7 weeks. After 7-week treatment with argan oil, blood lipoproteins were significantly reduced. Total cholesterol decreased with 36.67% (P<0.01), low density lipoprotein (LDL)-cholesterol in 67.70% (P<0.001), triglycerides in 30.67% (P<0.05) and body weight in 12.7% (P<0.05). High density lipoprotein (HDL)-cholesterol concentration remained unaltered. These results indicate the beneficial effect of argan oil in the treatment of the hyperlipidemia and hypercholesterolemia. This effect will be related with the polyunsaturated fatty acids and other constituents of studied oil.

Relaxant activity of methanolic extract from seeds of Peganum harmala on isolated rat aorta.

The activity of methanolic extract from the seeds of Peganum harmala L. (MEP) on vascular smooth muscle (rat aorta) was investigated. MEP induced relaxation in aorta precontracted with noradrenaline (10(-6) M) or KCl (80 mM) (IC50 = 14.49 +/- 1.15 and 5.93 +/- 1.26 micrograms/mL, respectively) in a dose-dependent manner and this relaxant effect was not endothelium-dependent. The vasodilatory effects were potentiated by isoprenaline (10(-9) M) (1.08 +/- 0.14 micrograms/mL) and negatively affected by a non-specific inhibitor of phosphodiesterase, IBMX (10(-4) M) (20.81 +/- 1.06 micrograms/mL). Pretreatment with MEP (3, 6, 18 micrograms/ml) shifted the phenylephrine-induced dose-response curves to the right and the maximum response was attenuated, indicating that the antagonist effect of MEP on alpha 1-adrenoceptors was non-competitive. These results suggest that MEP exerts a vasodilatory effect not related to the presence of endothelium and the main mechanism may be related to the inhibition of cyclic AMP phosphodiesterase.