Pomegranate (Punica granatum L.) juice (PJ) contains different types of antioxidants and bioactive polyphenols and has been reported to promote cardiovascular health through several mechanisms. The present study aimed to examine the effects of 2-week intake of fresh PJ on blood pressure, flow-mediated dilatation (FMD), serum lipid profile and concentrations of inflammatory and endothelial function biomarkers. Twenty-one hypertensive patients (aged 30-67 years) were recruited into the trial and assigned to receive either PJ (150 ml/day in a single occasion between lunch and dinner; n = 11) or the same amount of water (n = 10) for a period of 2 weeks. Systolic (SBP) and diastolic (DBP) pressures together with FMD and serum concentrations of lipid profile parameters, apolipoproteins A and B, intracellular adhesion molecule-1 (ICAM-1), vascular endothelial adhesion molecule 1 (VCAM-1), E-selectin, high-sensitivity C-reactive protein (hs-CRP) and interleukin-6 (IL-6) were measured at baseline and at the end of trial. PJ consumption was associated with significant reductions in SBP (p = 0.002) and DBP (p = 0.038) but not FMD (p > 0.05). Serum levels of VCAM-1 (p = 0.008) were significantly reduced by PJ while those of E-selectin were elevated (p = 0.039). However, no significant effect was observed from PJ on serum levels of ICAM-1, hs-CRP, lipid profile parameters, apolipoproteins and IL-6 in any of the study groups (p > 0.05). Consumption of PJ for 2 weeks has effective hypotensive effects, and may improve endothelial function by decreasing serum concentrations of VCAM-1. These findings suggest PJ as a beneficial cardioprotective supplement for hypertensive subjects.

Aim: Herein, the AS1411 aptamer-targeted ultrasmall gold nanoclusters (GNCs) were assessed at different aspects as a radiosensitizer. Materials & methods: AS1411 aptamer-conjugated gold nanoclusters (Apt–GNCs) efficacy was evaluated at cancer cells targeting, radiosensitizing effect, tumor targeting, and biocompatibility in breast tumor-bearing mice. Results: Flow cytometry and fluorescence microscopy exhibited more cellular uptake for Apt–GNCs in comparison with GNCs. In addition, inductively coupled plasma optical emission spectrometry results demonstrated its effective tumor targeting as the tumors’ gold content for GNCs and Apt–GNCs were 8.53 and 15.33 μg/g, respectively. Apt–GNCs significantly enhanced radiotherapy efficacy as mean tumors’ volume decreased about 39% and 9 days increase in the mice survival was observed. Both GNCs and Apt–GNCs were biocompatible. Conclusion: The Apt–GNCs is a novel and efficient  radiosensitizer.

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Aims:Endothelial dysfunction is considered a sign of the early vascular changes preceding atherosclerosis. We studied the alteration of von Willebrand Factor (vWF), C -reactive protein (CRP), nitrite and Vascular Endothelial Growth Factor (VEGF) in a dietary reversal model of hypercholesterolemia in rabbit.Methods: This project was designed in two phases. In phase I, male rabbits (n = 11) were fed a 1% high cholesterol diet for 30 days. Then the diet was replaced with normal rabbit chow for other 30 days (cholesterol withdrawal phase, phase II). To compare the fatty streak formation with normal condition, a control group (n = 6) received normal diet during the study. The serum lipid levels, vWF, CRP, nitrite, and VEGF were measured before the experiment and by the end of each phase. Fatty streak formation in the walls of the aortas in both groups (high cholesterol diet and control group) was determined using intima thickness/media thickness (IMT) ratio.Results: The results indicate that the level of cholesterol, Low Density Lipoproteins (LDL), vWF and CRP increased signifi cantly in phase I, and decreased after hypercholesterolemic diet withdrawal (p < 0.05). No statistically signifi cant changes were found in VEGF levels but the serum level of nitrite increased signifi cantly during both phases of the study (p < 0.05). The IMT ratio in the walls of aortas was signifi cantly diff erent between the groups in both phases of studies (p < 0.05). There was a signifi cant correlation between nitrite and cholesterol levels in both phases (r = 0.62 and r = 0.98, p < 0.05). Nitrite concentration also correlated with IMT ratio in both phases of the study (r = 0.75 and r = -0.99, p < 0.05). vWF did not correlate with cholesterol but it correlated with IMT ratio in both phases of the study (r = 0.87 and r = 0.84, p < 0.05). CRP only correlated with cholesterol in the fi rst phase (r = 0.91, p < 0.05).Conclusions: Among the endothelial biomarkers, vWF was found to be a biological marker for identifying the risk of developing atherosclerosis; however a single biomarker may not provide appropriate information.

Background: Angiogenesis plays an important role in maintaining adequate oxygen delivery, and nitric oxide (NO) is a potential regulator of angiogenesis. NO is synthesized through three isoforms of NO synthase (NOS). It is hypothesized that the NO derived from inducible NOS (iNOS) may promote survival of ischemic tissue through angiogenesis. To test this hypothesis, we investigated the effect of iNOS deficiency (by L-NIL) on angiogenesis in a hindlimb ischemia model.Methods: Thirty-two male wistar rats randomly divided into four groups. In groups 1 & 2, hindlimb ischemia was induced by ligation of femoral artery and they received L-NIL and saline respectively. The animals in groups 3 and 4 also received L-NIL and saline respectively without surgical procedure. After 21 days, the serum concentration of nitrite, capillary density and expression of HIF1α were determined.Results: Serum nitrite levels were significantly lower in L-NIL groups (p<0.05). The capillary density in group 1 (ischemia + L-NIL) was significantly different from group 2 (ischemia + saline); group 1: 360.33 ± 77.02, group 2: 549 ± 81.85 /mm 2 , p<0.05) .In addition, expression of HIF1α was significantly increased in ischemic groups (p<0.05). Conclusion: Selective inhibition of iNOS by L-NIL inhibits angiogenesis in a hindlimb ischemic rat model. In addition, ischemia induces expression of HIF1α in hypoxic tissue.