RESUMEN
Objective To explore the characteristics of the interactions between traditional laxative medicine Cannabis Fructus and human gut microflora. Methods HPLC method was used to determine the content of the main unsaturated fatty acids linoleic acid and linolenic acid in Cannabis Fructus Decoction. At the same time, solid culture and liquid culture in vitro anaerobic culture method were combined with 16 S rRNA technology to analyze the interactions between Cannabis Fructus Decotion and human gut microflora. Moreover, the metabolits of linoleic acid and linolenic acid in Cannabis Fructus Decoction by human intestinal microflora were determined using HPLC method. At the same time, the possible conjugated linolenic acid and linoleic acid were determined. Results Cannabis Fructus Decoction promoted the growth of Proteobacteria significantly, which showed that Escherichia-shigella was significantly increased (P < 0.01), but the growth of Bacteroidetes was decreased (P < 0.01), and the content of unsaturated fatty acids linoleic acid and linolenic acid in Cannabis Fructus Decoction were reduced after being incubated with human intestinal bacteria, and the metabolites were conjugated linoleic acid and conjugated linolenic acid. Conclusion The interactions between Cannabis Fructus Decoction and human intestinal microflora are obvious. The Chinese medicine can change the structure of the gut microflora, and the gut microflora can metabolize the drug components. This analysis method partially restores the pharmacokinetics process of the oral administration drug in the human intestinal tract. It could provide a new insight of the mechanism research of Cannabis Fructus.
RESUMEN
Cancer chemoprevention utilizing food components is attracted because of its easily availability in humans. Bitter melon (<i>Momordica charantia</i>) (BMO) and pomegranate (<i>Punica granatum</i> L.) (PGO) seed oils contain a large amount of conjugated linolenic acid (CLN). In the first we demonstrated that BMO inhibits the development of azoxymethane (AOM)-induced putative precursor lesions for colonic adenocarcinoma in rats. Subsequently, we investigated the modifying effects of dietary administration of BMO or PGO on the development of colonic neoplasms using an animal colon carcinogenesis model initiated with a colon carcinogen AOM. Male F344 rats were given two weekly subcutaneous injections of AOM (20 mg/kg body weight) to induce colonic neoplasms. They were fed with the diets containing 0.01%, 0.1% and 1% BMO or PGO during the entire experimental period (for 32 weeks), starting one week before the first dosing of AOM. At the end of the study, the incidence and multiplicity of colonic adenocarcinoma were reduced in the "AOM+BMO" and "AOM+PGO" groups, when compared with the "gAOM alone" group. The contents of conjugated linoleic acid (CLA: 9<i>c</i>,11<i>t</i>-18:2) in the liver and colonic mucosa of rats fed BMO or PGO were elevated in a dose-dependent manner. Also, dietary BMO or PGO enhanced expression of peroxisome proliferator-activated receptor (PPAR)γ protein in the colonic mucosa. These findings may suggest that BMO or PGO rich in CLN can suppress AOM-induced colon carcinogenesis through the modification of lipid composition in the colon and liver and/or increased expression of PPARγ protein level in the colon mucosa. Our results might provide scientific evidence of an effective dietary chemopreventive approach using BMO and PGO seed oils rich in CLN to cancer chemoprevention, especially colon cancer development.<br>