Cacao polyphenols, catechins and procyanidins have attracted interest because of their possible effect on cardiovascular health. This paper provides an overview of our research on the effects of cocoa polyphenols on low-density lipoprotein (LDL) oxidizability and atherosclerosis. Polyphenol rich cocoa ingestion prolonged lag time (an index of LDL oxidative susceptibility) and decreased plasma oxidized LDL levels in humans and prevented atherosclerotic lesion formation in experimental animals. Catechins in cocoa show high bioavailability, and approximately 25-30% of ingested catechins are detectable in urine. After oral supplementation, they are present in blood as metabolites such as glucuronides and/or sulfate conjugated and/or methylated forms. The catechin metabolites (glucuronides) of rats and humans are structurally completely different, and their antioxidative activity is relatively maintained in rats but not in humans. On the other hand, ingestion of cacao products increased the level of HDL. The up-regulation of HDL might be shown antioxidative effect. Thus, cacao polyphenols may reduce cardiovascular disease risk.

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Matrix metalloproteinases (MMPs) are considered to be important for cardiovascular disease and nearly associated with the loss of renal function by diabetes mellitus. Green tea catechins inhibit mRNA expression and activity of MMPs in vitro study. We investigated in vivo study whether oral green tea administration could cause a change of MMPs in diabetic rats. Experimental diabetes was induced by single injection of 50 mg/kg streptozotocin (STZ) via the tail vein. The diabetic rats were fed on a green tea-free diet or 5% green tea-containing diet for four weeks. After four weeks, green tea ingestion significantly decreased the HbA1c level in STZ-induced diabetic rats (STZ rats). The activities of MMP-2 and MMP-9 in plasma determined by zymography significantly increased in diabetic rats compared with those of control rats, though both activities showed no change by green tea ingestion. The mRNA expression of MMP-2, MMP-9, tissue inhibitor of metalloproteinases (TIMP)-1 and TIMP-2 in rat whole kidney, was determined by RT-PCR. The mRNA expression of MMP-9 and TIMP-1 significantly decreased in diabetic rat kidney compared with control rat, but green tea ingestion in diabetic rats (STZ+GT rats) allowed both expressions to recover to control level. MMP-2 and TIMP-2 mRNA expression in STZ+GT rats significantly increased compared with control rats and STZ rats. Thus, feeding with 5% green tea-containing diet improved the impairment of MMP regulation in STZ-induced diabetic rat kidney.

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The present study was designed to investigate the hepatoprotective effect of 2% chitin-chitosan mixture on high fat diet-induced fatty liver, an experimental model for non-alcoholic fatty liver disease, in Wistar strain male rats. The hepatoprotective property was determined based on the following criteria: total lipid in liver, concentrations of total cholesterol, triglycerides, free fatty acids and phospholipids of serum and liver tissue; liver lipid/protein ratio; serum and tissue activities of aspartate amino transferase (AST) and alanine amino transferase (ALT); fecal fat determination and activity of pancreatic lipase. Chitin-chitosan fed animals gained less weight compared to the controls. A significant (p < 0.001) reduction in the liver lipid/protein ratio was observed in chitin-chitosan mixture supplemented rats as compared to that of control animals. Also the blood and liver fat, cholesterol, triglycerides, free fatty acids and phospholipid concentrations, decreased significantly by chitin-chitosan supplementation. Serum levels of aspartate aminotransferase and alanine aminotransferase showed significant (p < 0.001) reduction while tissue levels exhibited a concomitant increase upon chitin-chitosan treatment. Enhanced fat excretion (p < 0.001) was observed in the chitin-chitosan supplemented group. In the present study, supplementation of chitin-chitosan mixture did not induce any significant change in the activity of pancreatic lipase as compared to normal animals. This indicates that the antilipidaemic effect of chitin-chitosan mixture supplementation was mainly due to the interference in the gastrointestinal absorption of dietary fat rather than the mixture having any direct role on lipid metabolism. In conclusion, dietary supplementation of chitin-chitosan mixture can alleviate the high fat diet-induced aberrations related to lipid metabolism in fatty liver of experimental animals by their antilipidaemic property.

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To elucidate the efficacy of dietary therapy for ulcerative colitis (UC), we analyzed the dietary fatty acid intakes, fatty acid compositions of phospholipids in the plasma and blood cells, and serum cytokines of 12 patients with UC. Correlations among fatty acid compositions in the diet, blood cell phospholipids and serum cytokines were also investigated in UC patients. Although the fat energy ratio was lower in the UC patients than in the controls, no significant difference was observed in their fatty acid intakes. Significantly higher linoleic acid levels were observed in the erythrocyte, mononuclear cell and neutrophil phospholipids of the UC patients compared with the controls. Concerning neutrophil phospholipids, two times higher levels of linoleic acid and arachidonic acid and lower levels of eicosapentaenoic acid (EPA) were observed in the UC patients compared with those in the controls. The serum TNF-α concentration was correlated positively with molar percentage of linoleic acid (r = 0.675, p < 0.02) and negatively with the n-3 polyunsaturated fatty acid (PUFA) (r = -0.584, p < 0.05) in the plasma phospholipids of UC patients. Dietary EPA intake was correlated negatively with the n-6 PUFA molar percentage in the phospholipids of the plasma, mononuclear cells and neutrophils. From these findings, we suggest that a diet high in n-3 PUFA and low in linoleic acid should be recommended for UC patients.

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Changes in gene expression and the enzymatic activity of inducible nitric oxide synthase (iNOS), heme oxygenase isoenzymes 1 and 2 (HO-1 and HO-2) and cyclic GMP (cGMP) tissue levels in the corpora cavernosa (CC) were investigated experimentally in sixty Sprague-Dawley rats subjected to either HO or NOS inducers or inhibitors. They were divided into 5 groups (n = 12/group): Control group, L-arginine group which received L-arginine as NOS inducer, L-nitroarginine methyl ester (L-NAME) group which received L-NAME as NOS inhibitor, Hemin group which received hemin as HO inducer and Zn protoporphyrin (ZnPP) group which received ZnPP as HO inhibitor. The results of this study demonstrated that there was co-induction as well as co-repression of iNOS and HO-1 gene expression using either the inducers or inhibitors of both enzymes, whereas HO-2 gene expression was found to be upregulated by the use of L-arginine only in L-arginine rat group. HO-2 gene expression was not changed by the use of either HO inducer, suppressor or NOS suppressor. cGMP tissue levels in CC was significantly elevated in rats receiving HO inducer (hemin) as well as in those receiving NOS inducer (arginine) as compared with the control group, with a significant elevation in cGMP levels in hemin group as compared with L-arginine group. The use of hemin appears to be more efficient and dominates the use of arginine in inducing HO activity as well as cGMP tissue levels. These data indicate that HO and its product carbon monoxide (CO) are supervising nitric oxide as a signaling molecule in erectile function. On the other hand, There was a significant decrease in cGMP levels in HO inhibitor and in NOS inhibitor groups with a significant decrease in its levels in ZnPP group as compared with L-NAME group. HO enzymatic activity was significantly elevated in the hemin group, whereas it was significantly decreased in ZnPP and in arginine rat groups in comparison with the other groups. NOS activity was significantly elevated in arginine group and in ZnPP group and it was significantly decreased in L-NAME and in hemin rat groups in comparison with the other rat groups. Conclusion: The use of either NOS or HO inducers can equally enhance erectile function via upregulation of gene expression of the two signaling genes involved in erection as well as through upregulation of the tissue levels of cGMP, the mediator of vasodilatation. Our data indicate that HO/CO system is supervising and dominating nitric oxide as a signaling molecule in erectile function. Thus, induction of HO may have therapeutic implications for management of erectile dysfunction.

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