Hempseed is a novel functional food that contains several health-promoting polyunsaturated fatty acids (PUFAs). PUFAs, such as those found in flaxseed and fish, have been shown to protect the heart against arrhythmias following ischemia/reperfusion.TO INVESTIGATE THE POTENTIAL OF DIETARY HEMPSEED AS A CARDIOPROTECTIVE AGENT AGAINST GLOBAL ISCHEMIA AND SUBSEQUENT REPERFUSION BY ASSESSING SEVERAL MEASUREMENTS OF CARDIAC PERFORMANCE: QT interval duration, left ventricular pressure, arrhythmia incidence and arrhythmia duration.MALE NEW ZEALAND WHITE RABBITS WERE FED ONE OF SIX DIETS: a control diet; or one supplemented with 10% hempseed, 10% delipidated hempseed, 0.5% cholesterol, 0.5% cholesterol plus 10% hempseed or 5% coconut oil. After eight weeks on their respective diets, the hearts were excised and subjected to 30 min of global ischemia and 45 min of reperfusion. Electrocardiogram traces were recorded throughout the experiment and were subsequently analyzed for QT interval duration, left ventricular pressure, arrhythmia incidence and arrhythmia duration. Plasma and cardiac tissue were analyzed for fatty acid content and composition.Cholesterol-fed animals exhibited significantly higher PUFA levels in their plasma, but this did not directly translate into higher PUFA levels in their cardiac fractions. There were no significant differences among the groups in the incidence or duration of ischemia-derived arrhythmias. During reperfusion, there was a significant decrease in the incidence of fibrillation in the hearts obtained from cholesterol-fed and hempseed- plus cholesterol-fed rabbits compared with the hearts from delipidated hempseed-fed rabbits.Dietary hempseed induced limited beneficial effects on cardiac function during ischemia/reperfusion challenge. The present study does not support the use of dietary hempseed to protect the heart during ischemic insult in this experimental model.

Objective— Our study tested the hypothesis that the mitogenic effect of oxidized low-density lipoprotein (oxLDL) on vascular cells may be further enhanced by the presence of cytokines and growth factors known to be present in the atherosclerotic environment. Methods and Results— Quiescent fibroblasts and vascular smooth muscle cells were treated with 10 or 50 μg/mL minimally-oxidized LDL in combination with serum for 24 or 48 hours. Surprisingly, these cells showed inhibited release from growth arrest and a significant reduction in the number of cells completing the cell cycle when compared with cells treated with serum alone. This was not due to an induction of apoptosis. The antiproliferative effects were not closely associated with changes in the expression of cell cycle proteins. Instead, oxLDL inhibited the translocation of cell cycle proteins cell division cycle (Cdc) 2, cyclin-dependent kinase (Cdk) 2, Cdk 4, Cyclin A, Cyclin B1, Cyclin D1, and proliferative cell nuclear antigen (PCNA) into the nucleus, as compared with separate treatments with serum alone. Kinase activation associated with specific cell cycle proteins was also inhibited by oxLDL. Conclusions— oxLDL, in the presence of serum, has a surprising inhibitory effect on cell proliferation that occurs through an inhibition of import of cell cycle proteins into the cell nucleus.

Oxidized low-density lipoprotein (oxLDL) may be involved in atherosclerosis by stimulating proliferation of cells in the vessel wall. The purpose of this study was to identify the mechanism by which oxLDL induces proliferation. Quiescent human fibroblasts and rabbit smooth muscle cells were treated with 0, 10, or 50 microg/ml oxLDL for 24-48 h. This resulted in significant increases in total cell counts at both concentrations of oxLDL, at both time points, for both types of cells. Western blot analysis revealed that oxLDL-stimulated cell proliferation was associated with significant increases in the expression of proteins that regulate entry into and progression through the cell cycle [cell division cycle 2, cyclin-dependent kinase (cdk) 2, cdk 4, cyclin B1, cyclin D1, and PCNA]. Surprisingly, the expression of cell cycle inhibitors (p21 and p27) was stimulated by oxLDL as well, but this was to a lesser extent than the effects on cell cycle-activating proteins. OxLDL also induced nuclear localization of all cell cycle proteins examined. The similar effects of oxLDL on the translocation and expression of both cell cycle-activating and -inhibiting proteins may explain the controlled proliferative phenomenon observed in atherosclerosis as opposed to the more rapid proliferative event characteristic of cancer.