Favorable impact of Nigella sativa seeds on lipid profile in type 2 diabetic patients

The atherogenic pattern of dyslipidemia associated with type 2 diabetes mellitus [DM] has been increasingly discussed. We have recently reported a hypoglycemic effect of Nigella sativa [NS] seeds in patients with type 2 DM. In this study we sought to assess the impact of NS seeds on lipid profile in type 2 diabetic patients. A total of 94 patients with type 2 DM were recruited and divided into 3 dose groups. Capsules containing NS were administered orally in a dose of 1, 2, and 3 g/day for 12 weeks. All patients were subjected to measurement of total cholesterol [TC], triglycerides [TG], low-CJ density lipoprotein cholesterol [LDL-c], and high-density lipoprotein cholesterol [HDL-c] before treatment and 4, 8, and 12 weeks thereafter. Patients receiving 1 g/day NS seeds for 12 weeks [group 1] showed I nonsignificant changes in all the parameters except for a significant increase in HDL-c after 4 weeks of treatment. However, patients ingested 2 g/day NS displayed a significant decline in TC, TG, and LDL-c, and CD a significant elevation in HDL-c/LDL-c, compared with their baseline data and to group 1 patients. Increasing

Differential effects of vitamin E supplementation on cardiovascular risk factors and on cardiac vulnerability to ischemia and reperfusion in rats

The present study was performed to examine the effects of vitamin E on hemodynamics, electrocardiogram [ECG] pattern, plasma levels of lipid profile, enzymes reflecting myocardial cell integrity creatine kinase [CK] and lactate dehydrogenase [LDH] and rate of lipid peroxidation as well as on myocardial performance after ischemia-reperfusion injury in isolated rat hearts. Vitamin E-treated rats were injected with vitamin E in a dose of 4 mg/100g body weight [b.w.] daily, for 6 consecutive days. Control rats were treated with vitamin E-solvent, daily, for the same duration. Then, rats were sacrificed, and the isolated heart were subjected to 30 min. ischemia followed by 30 min period of reperfusion. The present study demonstrated that administration of vitamin E in normal rats did not produce any appreciable hemodynamic effects as regards heart rate [HR], mean arterial pressure [MAP,], and pressure rate product[PRP]. The ECG pattern showed no arrhythmias or ischemic changes compared to control group. Concerning changes in plasma lipid profile, vitamin E-treated rats showed significant reduction in both total cholesterol [TC], and low density lipoprotein-cholesterol [LDL-C] Moreover, high density lipoprotein-cholesterol / total cholesterol [HDL-C/TC] was significantly elevated, in contrast to a non significant decrease in both low density lipoprotein-cholesterol/ total cholesterol [LDL-C /TC] and LDL-C /HDL-C ratios, when compared with controls. Myocardial cellular integrity, estimated by the plasma level of CK and LDH, was preserved by the administration of vitamin E, revealed evidently by the significant decrease in CK and LDH release in plasma of rats treated with vitamin E as compared to control rats. Moreover, the plasma level of malondialdehyde, as an index for the degree of lipid peroxidation, was significantly reduced. The preischemic, baseline activity of the isolated hearts obtained from rats treated with vitamin E, revealed non significant changes in myocardial inotropy except for prolongation of half relaxation time. Also there was a significant reduction in both heart rate and LDH release in the coronary effluent, while there was a non significant change in tile coronary flow rate. The results of the isolated hearts subjected to reperfusion following 30 minutes ischemic period, showed that vitamin E decreased the detrimental effect of reperfusion on the inotropic activity observed in the control group, evident by superior recovery of postischemic reperfusion myocardial functions. Manifested by elevated peak developed tension, and tension generation per unit time, concomitant with shortening of time to peak tension, and half relaxation time, along the reperfusion period. In addition, the percentage recovery of the heart rate was better during the whole reperfusion period but the difference was statistically significant only at 15-minute of reperfusion, and as well myocardial flow rate percentage .showed significant superior recovery in vitamin E-treated rat hearts. Moreover, there was a significant reduction in both CK and LDH release in the coronary effluent of vitamin E treated rat hearts, compared to control hearts. It could be concluded that vitamin E administration has a favorable potential against the risk of atherosclerosis and lipid peroxidation and as well it may attenuate the detrimental effects of postischemic reperfusion on the myocardial contractility

Age-related changes in haemostatic responses to localized cold-induced stress in rats

In the present work, age-related changes in haemostatic responses to localized cold stress in rats were investigated. The role of vitamin E supplementation, on the haemostatic responses of those stressed rats, was also studied. Three different age groups were studied; young mature rats [4 months], middle-age rats [14 months] and old-age rats [24 months]. The animals were subjected either to acute localized cold stress [1 hour] or to chronic localized cold stress [3 hours daily, for 15 days]. Age-matched control rats were maintained under standard conditions of boarding. A group of old rats was injected intramuscularly by vitamin E in a dose of 150 mg/kg-body weight/day, prior to the stress induction [daily, for 15 days]. Exposure to acute localized cold stress produced a significant elevation in the mean arterial blood pressure in the three different age groups of rats, compared to their age matched controls. On the other hand, chronic exposure to localized cold stress resulted in significant elevation in the mean arterial blood pressure [MAP] and plasma malondialdehyde [MDA] level, with an increase in platelet aggregation, and a decrease in platelet count. In addition, there were shortening in prothrombin and partial thromboplastin times, as well as a reduction in antithrombin III activity and an increase in the levels of plasma fibrinogen and fibrin degradation products in all stressed rat groups, compared to their age matched unstressed controls. These platelet hyperaggregability and blood hypercoagulability states observed in stressed rats raise the risk of thrombo-embolic manifestations. Vitamin E supplementation in old rats subjected to chronic localized cold stress produced a significant decrease in MAP and plasma MDA level, as well as inhibited the activated coagulation system induced by cold exposure in old age, evidenced by decreased platelet aggregation in response to ADP and plasma fibrinogen level, in concurrence with prolonged PTT and stimulated AT-III activity compared to stressed old rats. Further, the value of all these parameters were corrected to near normal levels, being non significantly different from the corresponding values in the normal old rats. Therefore, the therapeutic intervention with vitamin E might improve the stress- induced derangement in the haemostatic profile

Age-related changes in haemostatic responses to oxidative stress

Altered haemostatic mechanisms are known to occur in stressful situations, yet the pathophysiology of stress related dyshaemostasis is still poorly understood. In the present work, age-related changes in haemostatic responses to oxidative stress in rats with different ages were investigated. Also, the effects of vitamin E supplementation, prior to stress induction, on the haemostatic responses of those stressed rats were evaluated. Three different age groups were studied, young mature rats [4 months], middle age [14 months] and old rats [24 months]. The animals were subjected to oxidative stress by adding H[2]O[2] solution to their drinking water, in a final concentration of 3%, daily, for 21 days. The age-matched control rats drink normal tap water. A group of old rats was injected intramuscularly by vitamin E in a dose of 150 mg/kg body weight, prior to the stress induction, daily, for 21 days.Results obtained in this study demonstrated an elevation in mean arterial blood pressure, plasma malondialdehyde, and plasma fibrinogen concentrations, and fibrin degradation products, in addition to shortened prothrombin and partial thromboplastin times and inhibited antithrombin III activity, in the young and old rats subjected to H[2]O[2]-induced oxidative stress, being statistically significant compared to their age matched controls. Moreover, there were an increase in platelet aggregation and a decrease in platelet count in the stressed young and old groups, but they were statistically significant only in old rats, compared to their age matched controls. However, stressed middle-age rats showed non-significant changes in the studied parameters, except for the mean arterial blood pressure that was significantly elevated, compared to their age matched controls. From these results, it is clear that the changes in the haemostatic responses to stress were more manifest in the young and old rats, with more marked responses in the older ones. On the other hand, vitamin E supplementation in old rats, prior to the stress induction, produced a decrease in mean arterial blood pressure, platelet aggregation, plasma fibrinogen concentration and fibrin degradation products, as well as increase in platelet count and antithrombin III activity. All these changes were statistically significant compared to the vitamin E-unsupplemented stressed old rats, but they were non significantly changed from the normal controls. It is concluded that vitamin E injection, prior to stress induction, produces marvelous effects on the stress-induced derangement of the haemostatic system