Recent research studies have shown that the intestinal flora are related to the occurrence and progress of breast cancer. This study investigates the effect of fucoidan on intestinal flora and intestinal barrier function in rats with 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast cancers. Sixty female Sprague-Dawley rats were randomly assigned to the control group, the model group, and the F1 and F2 groups, which were fed fucoidan at concentrations of 200 and 400 mg per kg bw (body weight), respectively. Intestinal histopathological analysis was performed and 16S rDNA high-throughput sequencing was used to provide an overview of the intestinal flora composition. The contents of D-lactic acid (D-LA), diamine oxidase (DAO) and endotoxin in plasma were detected by ELISA. Expression levels of the tight junction (TJ) proteins, phosphorylated p38 MAPK and ERK1/2 were measured using western blotting. Our results suggested that the intestinal wall of the model group was damaged. However, after fucoidan intervention, the villi were gradually restored. ELISA showed that the levels of plasma endotoxin, D-LA and DAO decreased in the F1 and F2 groups compared to those in the model group. Fucoidan treatment also increased the expressions of ZO-1, occludin, claudin-1 and claudin-8. Furthermore, the expression levels of phosphorylated p38 MAPK and ERK1/2 were upregulated in fucoidan treatment groups. The results of 16S rDNA high-throughput sequencing indicated that fucoidan increased the diversity of the intestinal microbiota and induced changes in microbial composition, with the increased Bacteroidetes/Firmicutes phylum ratio. In conclusion, the supplement of fucoidan could improve the fecal microbiota composition and repair the intestinal barrier function. The study suggested the use of fucoidan as an intestinal flora modulator for potential prevention of breast cancer.

Lactobacillus casei (L. casei), a kind of probiotics, is known as a “healthy triple benefit bacterium” along with Lactobacillus acidophilus and Bifidobacterium. L. casei is associated with the alteration of the intestinal flora population, and the gut microbiota–brain axis has been demonstrated to play an important role in many central nervous system diseases. The aim of this study was to evaluate the effectiveness of L. casei intervention in ameliorating mental disorders and potential mechanisms using a rat model with depression-like behaviour induced by chronic unpredictable mild stress (CUMS). L. casei intervention improved the CUMS-induced depression-like behaviors of rats, including a reduced body growth rate, decreased sucrose preference, increased immobility time, and lowered moving distance and velocity. In addition, L. casei intervention amended the gut microbiota structure changes induced by CUMS in rats. Furthermore, L. casei intervention reversed the CUMS-induced protein expression changes of monoamines dopamine, noradrenaline and 5-hydroxytryptamine, brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase receptor B (TrkB), and N-methyl-D-aspartic acid receptor 1, as well as CUMS-induced activations of ERK1/2 and p38 MAPK signal pathways. These findings suggested that L. casei could significantly protect against depression in rats, which was possibly associated with the alterations in the gut microbiota composition and mediation of BDNF–TrkB signaling.

NR treatment could protect against mice's alcohol-related depression-like behaviours, possibly by altering the composition of the gut microbiota.

Epidemiological studies have suggested inconclusive associations between 25-hydroxyvitamin D and total cancer incidence and mortality. The aim of this study was to quantitatively assess these associations by combining results from prospective cohort studies. A systematic literature search was implemented in PubMed and Scopus databases in April 2019. Comparing the highest with the lowest categories, the multivariate-adjusted relative risks (RRs) and the corresponding 95% confidence intervals (CIs) were pooled using a random-effects model. A trend estimation was performed using a two-stage, dose-response, meta-analysis method. Twenty-three independent prospective studies were included for data synthesis. Eight studies investigated the association between 25-hydroxyvitamin D and the risk of cancer incidence (7511 events and 70,018 participants), and the summary estimate showed that 25-hydroxyvitamin D is marginally associated with cancer risk (Summary RR = 0.86; 95% CI: 0.73, 1.02; I² = 70.8%; p = 0.001). Sixteen studies investigated the association between 25-hydroxyvitamin D and the risk of cancer mortality (8729 events and 101,794 participants), and a higher 25-hydroxyvitamin D concentration was inversely associated with the risk of cancer mortality (Summary RR = 0.81; 95% CI: 0.71, 0.93; I² = 48.8%, p = 0.012). Dose-response analysis indicated that the risk of cancer incidence was reduced by 7% (RRs = 0.93; 95% CI: 0.91, 0.96), and the risk of cancer mortality was reduced by 2% (RRs = 0.98; 95% CI: 0.97, 0.99), with each 20 nmol/L increment of 25-hydroxyvitamin D concentration. This meta-analysis provides evidence that a higher 25-hydroxyvitamin D concentration is associated with a lower cancer incidence and cancer mortality.