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. 2013 Apr 30;4(2):e0013.
doi: 10.5041/RMMJ.10113. Print 2013 Apr.

Pomegranate for your cardiovascular health

Michael Aviram  1 , Mira Rosenblat
Affiliations

Pomegranate for your cardiovascular health

Michael Aviram et al. Rambam Maimonides Med J. .

Abstract

Pomegranate is a source of some very potent antioxidants (tannins, anthocyanins) which are considered to be also potent anti-atherogenic agents. The combination of the above unique various types of pomegranate polyphenols provides a much wider spectrum of action against several types of free radicals. Indeed, pomegranate is superior in comparison to other antioxidants in protecting low-density lipoprotein (LDL, "the bad cholesterol") and high-density lipoprotein (HDL, "the good cholesterol") from oxidation, and as a result it attenuates atherosclerosis development and its consequent cardiovascular events. Pomegranate antioxidants are not free, but are attached to the pomegranate sugars, and hence were shown to be beneficial even in diabetic patients. Furthermore, pomegranate antioxidants are unique in their ability to increase the activity of the HDL-associated paraoxonase 1 (PON1), which breaks down harmful oxidized lipids in lipoproteins, in macrophages, and in atherosclerotic plaques. Finally, unique pomegranate antioxidants beneficially decrease blood pressure. All the above beneficial characteristics make the pomegranate a uniquely healthy fruit.

Keywords: Atherosclerosis; antioxidant; lipoproteins (LDL, HDL); macrophages; polyphenols; pomegranate.

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Figures

Figure 1.
Figure 1.
The effect of PJ consumption by patients with CAS on CIMT and on internal carotid EDV. Ten patients with CAS were supplemented with PJ for up to 1 year. Common CIMT and EDV were measured in the patients’ left and right carotid arteries before treatment (baseline) and during PJ consumption. The mean values of both carotid arteries are presented. The individual results of mean common carotid artery IMT, as well as the averages of all mean values ±SEM, are shown (A and B). The averages of all mean values ±SEM are shown for internal carotid artery EDV (C). *P<0.01 (after PJ consumption versus Baseline—“0” time).
Figure 2.
Figure 2.
The effect of PJ consumption by patients with CAS, or by diabetic patients, on their serum oxidative stress and on serum PON1 activity. A and C: Ten patients with CAS were supplemented with PJ for a 1-year period. Blood samples were drawn from the patients before, and after 3, 6, 9, and 12 months of PJ consumption. B and D: Ten patients with type 2 diabetes mellitus were supplemented with PJ for 3 months. Blood samples were drawn from the patients before, and after PJ consumption and also from 10 healthy subjects. A: The serum susceptibility to oxidation by 2,2′-azobis amidinopropane hydrochloride (AAPH) was determined by the lipid peroxides assay. B: Basal serum oxidative status was determined by the level of thiobarbituric acid reactive substances (TBARS). C and D: Serum PON1 arylesterase activity was measured using phenyl acetate as the substrate. Results are expressed as mean ±SD (n=10). *P<0.01 (after PJ consumption versus before treatment), ^P<0.01 (diabetic patients before versus healthy subjects), #P<0.01 (diabetic patients after PJ versus before).
Figure 3.
Figure 3.
The effect of PJ consumption by diabetic males on their HDL-associated PON1 activities. Ten male patients with type 2 diabetes mellitus consumed 50 mL of concentrated pomegranate juice (PJ) per day (which contain 1.5 mmol of total polyphenols) for a period of 1 month, followed by a period of 4 weeks’ “wash-out.” Blood samples were collected from the patients before (0 time) and 4 weeks after PJ consumption, as well as after the “wash-out” period. The HDL fractions were isolated from the blood samples of four patients by ultracentrifugation. The HDL-associated PON1 arylesterase (A), and lactonase activities (B) were determined. The individual results, as well as the mean±SD are shown.
Figure 4.
Figure 4.
The anti-atherogenic effects of PJ consumption on HMDM from diabetic patients, and on carotid lesions from patients with CAS. A and C: Monocytes were isolated from the blood of two healthy subjects and from three patients with type 2 diabetes before and after 3 months of PJ consumption (50mL per day). The monocytes were differentiated into macrophages in the presence of RPMI medium containing 10% autologous serum. After 7 days in culture the amount of ROS (A) and the uptake of Ox-LDL (20μg of protein/mL) labeled with FITC by the cells (C) were determined. Results are given as mean ± SEM.*P<0.01 diabetic patients’ HMDM versus healthy subjects’ HMDM, #P<0.01 diabetic patients’ HMDM after PJ consumption versus diabetic patients’ HMDM before PJ consumption. B and D: Lesions were collected from seven patients with CAS after endartherectomy and from two patients who consumed PJ for 3 and 12 months and had to undergo endartherectomy during the study, due to clinical deterioration. B: Lesions (0.3 g) were incubated with LDL (100 mg of protein/L) in PBS for 20 hours at 37°C. The extent of LDL oxidation was measured by the lipid peroxide assay. Lesion-mediated oxidation of LDL was calculated by subtracting the values obtained in control LDL (incubation with no lesion) from those obtained after LDL incubation with the lesions. Three determinations were done on each lesion. D: The amount of cholesterol was measured in the lesion homogenates. Results represent mean ± SEM. ^P<0.01 (carotid lesions after PJ consumption versus carotid lesions, no PJ).
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