Composition and safety evaluation of tea from New Zealand kawakawa (Piper excelsum).

Kawakawa (Piper excelsum) has food, medicinal and cultural importance to the indigenous Maori people of New Zealand, and is being incorporated into a range of commercial food and therapeutic products, including tea. In this study, the chemical compositions of kawakawa fresh leaves, dried leaves for tea, and hot brewed tea, were analysed and compared. The key metabolites were diayangambin, elemicin, myristicin, unidentified lignans and amides. The safety of brewed tea and tea leaves were evaluated in 8 week old Sprague Dawley rats in a 14 day acute study followed by a 28 day subacute study. In the 14 day study, the rats received the equivalent of 1, 2, 3 or 4 cups of kawakawa tea, and the rats in the 28 day study received daily doses that were equivalent to 4 cups per day. There were no adverse effects observed in the rats, and body weights and food intakes were not significantly different between the control and the kawakawa treated animals. There were small differences in organ weights, biochemical and haematology parameters observed in the rats given the kawakawa tea. In conclusion, the consumption of kawakawa tea could be considered safe within the conditions used in this study.

Dietary flavonoids from modified apple reduce inflammation markers and modulate gut microbiota in mice.

Apples are rich in polyphenols, which provide antioxidant properties, mediation of cellular processes such as inflammation, and modulation of gut microbiota. In this study we compared genetically engineered apples with increased flavonoids [myeloblastis transcription factor 10 (MYB10)] with nontransformed apples from the same genotype, "Royal Gala" (RG), and a control diet with no apple. Compared with the RG diet, the MYB10 diet contained elevated concentrations of the flavonoid subclasses anthocyanins, flavanol monomers (epicatechin) and oligomers (procyanidin B2), and flavonols (quercetin glycosides), but other plant secondary metabolites were largely unaltered. We used these apples to investigate the effects of dietary flavonoids on inflammation and gut microbiota in 2 mouse feeding trials. In trial 1, male mice were fed a control diet or diets supplemented with 20% MYB10 apple flesh and peel (MYB-FP) or RG apple flesh and peel (RG-FP) for 7 d. In trial 2, male mice were fed MYB-FP or RG-FP diets or diets supplemented with 20% MYB10 apple flesh or RG apple flesh for 7 or 21 d. In trial 1, the transcription levels of inflammation-linked genes in mice showed decreases of >2-fold for interleukin-2 receptor (Il2rb), chemokine receptor 2 (Ccr2), chemokine ligand 10 (Cxcl10), and chemokine receptor 10 (Ccr10) at 7 d for the MYB-FP diet compared with the RG-FP diet (P < 0.05). In trial 2, the inflammation marker prostaglandin E(2) (PGE(2)) in the plasma of mice fed the MYB-FP diet at 21 d was reduced by 10-fold (P < 0.01) compared with the RG-FP diet. In colonic microbiota, the number of total bacteria for mice fed the MYB-FP diet was 6% higher than for mice fed the control diet at 21 d (P = 0.01). In summary, high-flavonoid apple was associated with decreases in some inflammation markers and changes in gut microbiota when fed to healthy mice.

Cecal and colonic responses in rats fed 5 or 30% corn oil diets containing either 7.5% broccoli dietary fiber or microcrystalline cellulose.

Growing evidence suggests that microbiota in the human gastrointestinal tract play a crucial role in mediating the effects of foods on colonic health and host metabolism. The large bowel ecosystem is known to be perturbed in humans and animals fed high-fat diets and conversely to be protected by fermentable oligosaccharides. We examined the ability of largely fermentable dietary fiber from broccoli ( Brassica oleracea L. var. italica ) and minimally fermented microcrystalline cellulose to buffer against the effects of high-fat intakes. The results showed that high fat lowered food intakes and therefore fiber intake by 27%. The addition of fermentable oligosaccharide to the diet was shown to be beneficial to some microbiota in cecum, altered cecal short-chain fatty acids, and increased the colon crypt depth and the number of goblet cells per crypt in high- and low-fat diets. Although, the fat level was the predominant factor in changes to the large bowel ecosystem, we have shown that broccoli fiber conferred some protection to consumption of a high-fat diet and particularly in terms of colon morphology.

The effects of dietary curcumin and rutin on colonic inflammation and gene expression in multidrug resistance gene-deficient (mdr1a-/-) mice, a model of inflammatory bowel diseases.

Damage of the intestinal epithelial barrier by xenobiotics or reactive oxygen species and a dysregulated immune response are both factors involved in the pathogenesis of inflammatory bowel diseases (IBD). Curcumin and rutin are polyphenolic compounds known to have antioxidant and anti-inflammatory activities, but their mechanism(s) of action are yet to be fully elucidated. Multidrug resistance gene-deficient (mdr1a-/- ) mice spontaneously develop intestinal inflammation, predominantly in the colon, with pathology similar to IBD, so this mouse model is relevant for studying diet-gene interactions and potential effects of foods on remission or development of IBD. The present study tested whether the addition of curcumin or rutin to the diet would alleviate colonic inflammation in mdr1a-/- mice. Using whole-genome microarrays, the effect of dietary curcumin on gene expression in colon tissue was also investigated. Twelve mice were randomly assigned to each of three diets (control (AIN-76A), control +0.2% curcumin or control +0.1% rutin) and monitored from the age of 7 to 24 weeks. Curcumin, but not rutin, significantly reduced histological signs of colonic inflammation in mdr1a-/- mice. Microarray and pathway analyses suggested that the effect of dietary curcumin on colon inflammation could be via an up-regulation of xenobiotic metabolism and a down-regulation of pro-inflammatory pathways, probably mediated by pregnane X receptor (Pxr) and peroxisome proliferator-activated receptor alpha (Ppara) activation of retinoid X receptor (Rxr). These results indicate the potential of global gene expression and pathway analyses to study and better understand the effect of foods in modulating colonic inflammation.