Smoothy Slim
Smoothy Slim
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Because inflammation has an important role in atherosclerosis development, significant reduction in inflammatory lesion may be due to anti-inflammatory effect of apple juice. The protective effects of flavonoids against chronic diseases have been attributed to their free radical-scavenging property.
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Contains a potent powdered supplement blended right into water or your favored beverage to be appreciated as a scrumptious morning smoothy.
Learn More »The significant decrease in CRP, fibrinogen, factor VII, TC, TG, LDL-C and the significant increase in nitrite, nitrate and HDL-C in rabbits receiving apple juice as compared to the high-cholesterol group represent that this extract is effective in moderating the dyslipidemic condition arising from a high cholesterol diet. Histological results indicate that apple juice significantly reduced atherosclerotic lesions of coronary arteries, when compared to the high-cholesterol groups. In our study, nitrite and nitrate increased in high cholesterol control compared to normal diet. It has been suggested that enhanced NO synthesis might be a defense mechanism to compensate for continuous inactivation of NO and protection against damaging factors [20]. The proposed mechanism responsible for the increase of nitrite and nitrate may be a significant increase in overall NOS synthesis by other cell types (than endothelium) in advanced lesions composed of the endothelial, neuronal and inducible isoforms of nitric oxide synthase (iNOS) enzymes [21]. Both low and high-doses apple juice with cholesterolemic diet caused significant increase in nitrite and nitrate compared with high cholesterolemic diet. The release of nitric oxide (NO) by a healthy vascular endothelium, which consists of a single layer of endothelial cells, prevents the adherence of platelets and leukocytes to the arterial wall. Therefore, reducing platelet activity could reduce athero-thrombotic events [22]. In addition to its antiatherogenic properties, NO also stimulates the vascular smooth muscle to relax and produce vasodilation. However, the endothelium can be damaged by many of the known vascular disease risk factors such as hypercholesterolemia, hypertension, and diabetes, thus reducing the bioavailability of NO[23]. The release of ROS is increased in states of oxidative stress and neutralizes the beneficial effects of NO by converting it to peroxynitrite [24]. The increase in NO and decrease in ROS attenuate multiple mechanisms that are central to the development and progression of atherosclerosis. The biological activity of NO can be effectively increased by the scavengers of oxygen-free radicals [25]. However, polyphenolic compounds can increase the NO releasing by two mechanisms: 1-Stimulation of NO synthase activity and preservation or stabilization of NO release under basal conditions. 2- Protection of NO from destruction by superoxides and other free radicals [26]. Schuldt EZ et al reported that polyphenols were able to scavenge free oxygen radicals to a limited extent resulting in an increased NO level [26]. Diets rich in dealcoholyzed red wine (DRW), quercetin or catechin induced endothelium-dependent vasorelaxation in rat aorta in a resting state through the enhancement of NO production, without modifying O2- generation, thus the bioavailability of NO was increased. The increase in the NO-cyclic GMP pathway explains the beneficial effect of flavonoids at vascular level [27]. Following concurrent use of 5 and 10 ml apple juice with cholesterolemic diet, fibrinogen and factor VII levels were significantly decreased in comparison with high-cholesterol group. Studies show that red wine consumption caused significant decreases in fibrinogen and factor VII [28, 29]. In a study by Grenett HE et al in rats, the impact of polyphenols on expression of fibrinolytic protein [urokinase-pA(u-PA), (t-PA), (PAI-1)] mRNAs in endothelial cells of aorta was evaluated. The expression of t-PA and u-PA mRNA was up-regulated, but conversely PAI-1 mRNA expression was down-regulated by both ethanol and polyphenols including catechin and quercetin. As a result, the firbrinolysis was increased in rat endothelial cells, an effect which might exert a beneficial cardio protective role [30].
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Learn More »The individual polyphenols of apple juice and ciders were examined for their ability to inhibit tissue activator, urokinase and plasmin. Neither phloridzin nor chlorogenic acid had any inhibitory activity at concentrations of 500 micrograms/ml while epicatechin had only a slight inhibitory effect at this concentration [31]. Using both doses of apple juice with cholesterolemic diet induced a significant decrease in CRP compared to hypercholesterolemic diet. In high cholesterol group, CRP was increased significantly compared to the normal diet group; however it has been shown in another studies with hypercholesterolemic rabbits [32, 33]. C-RP may actively promote atherogenesis [34], causing lesion formation via mechanisms such as endothelial dysfunction and leukocyte activation [35] and changes in plaque structure resulting in stability reduction and enhancing rupture. Many reviews aimed to study the effects of flavonoids on inflammatory processes [36] which showed that they may inhibit some active enzymes during the inflammatory process [37]. Isoforms of iNOS and of cyclooxygenase (COX-2) are responsible for the production of prostaglandins and nitric oxide biosynthesis which act as a mediators. In vitro studies have demonstrated that nitric oxide production and the expression of iNOS inhibit by flavonoid quercetin [38]. Flavonoids can modulate the molecular events cascade in several critical steps resulted in iNOS or COX-2 over expression. It seems that activation of a transcription essential for the expression of proinflammatory genes, the nuclear factor kappa B (NF-kappa B)converge the iNOS and COX-2 induction pathways [39]. Some of inducible transcription factors can constitute potential key targets for the treatment of the inflammation and NFkappaB is one of the most important of them which can trigger a cascade of molecular events by its modulation. It is showed that CRP protein level in hepatic cells may reduce by diverse flavonoides and that the effect is dose-dependent [40]. Studies indicated that CRP can be induced by IL-6 mechanism that involves NF-kappaB activation [41, 42]. An inhibition of the nuclear NF-kappaB translocation and of CRP synthesis in hepatocytes can cause by alterations in the intracellular state redox [43]. So it is possible that effects of flavonoids on CRP expression could be mediated, at least partly, by the modulation of the NF-kappaB-dependent pathway. Results of Golzarand M et al showed that ingestion of apple cider vinegar in patients with type 2 diabetes had no effect on CRP but it reduced IL-6 concentrations [44]. Findings of Chung OK, et al demonstrated that intake of dietary flavonoids is inversely associated with serum CRP concentrations in U.S. adults. Intake of flavonoid-rich foods may reduce inflammation-mediated chronic diseases [45]. Studies of Terra X, et al indicated that the procyanidins of grape seed decrease plasma CRP levels in rat. The decrease in plasma CRP in hypercholesterolemic rats is related to a down-regulation of CRP mRNA expression in the liver [46].
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Learn More »We showed that dietary consumption of 5 and 10 ml apple juice with cholesterol diet significantly decreased serum TC and TG. Aprikian O, et al [2001] found that when cholesterol fed rats were supplemented with lyophilized apples, there was a significant drop in plasma cholesterol and liver cholesterols and an increase in high-density lipoproteins (HDL). Furthermore, they found that cholesterol excretion increased in the feces of rats fed apples, suggesting reduced cholesterol absorption [47]. Also, Aprikian O, et al [2003] in more recent studies, found that combined apple pectin and apple phenolic fractions lowered plasma and liver cholesterol, triglycerides, and apparent cholesterol absorption to a much greater extent than either apple pectin alone or apple phenolics alone [48]. Histological results indicate that apple juice intake reduced atherosclerotic lesion in coronary vessels significantly with compared to hypercholesterolemic group. Because inflammation has an important role in atherosclerosis development, significant reduction in inflammatory lesion may be due to anti-inflammatory effect of apple juice. The protective effects of flavonoids against chronic diseases have been attributed to their free radical-scavenging property. In the case of CVD, flavonoids have been shown to reduce low density lipoprotein (LDL) oxidation, an important step in atherogenesis [49, 50]. Hung MT, et al [51] has suggested that polyphenolic compounds inhibit proinflammatory cytokines expression including IL-6, IL-1 and CRP expression. Apple was identified as a major dietary source of flavonoids especially flavan-3-ols (catechins) in the epidemiologic studies that inhibits cyclooxygenase enzymes [52, 53] that produce inflammation and stimulate inflammatory responses in body [54]. Studies by Decorde K, et al indicated that phenols of grape, apple and their juices reduce atherosclerosis lesion in hamster. This value was reduced by %93 in grape juice,%78 in purple grape,%60 in apple juice and %48 in apple[16]. In study performed by Da Luz PL, et al on the effect of red wine on experimental atherosclerosis, the rabbits that given red wine had significantly less atherosclerotic plaque development in their arteries than those not given wine at all[55]. In conclusion, results of this study suggest that hypercholesterolemic atherosclerosis is associated with an increase in oxidative stress in coronary arteries and that apple juice is effective in reducing hypercholesterolemic atherosclerosis by lowering levels of fibrinogen, VII, CRP, TC, TG, LDL-C and raising levels of nitrite, nitrate and HDL-C. Therefore, apple juice may be useful in preventing hypercholesterolemic atherosclerosis and lowering the related risk of coronary artery disease.
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