Age-Related Response of Rumen Microbiota to Mineral Salt and Effects of Their Interactions on Enteric Methane Emissions in Cattle.

Mineral salt bricks are often used in cow raising as compensation for mineral losses to improve milk yield, growth, and metabolic activity. Generally, effects of minerals are partially thought to result from improvement of microbial metabolism, but their influence on the rumen microbiota has rarely been documented to date. In this study, we investigated the response of microbiota to mineral salt in heifer and adult cows and evaluated ruminal fermentation and enteric methane emissions of cows fed mineral salts. Twelve lactating Holstein cows and twelve heifers fed a total mixed ration (TMR) diet were randomly allocated into two groups, respectively: a treatment group comprising half of the adults and heifers that were fed mineral salt and a control group containing the other half fed a diet with no mineral salt supplement. Enteric methane emissions were reduced by 9.6% (P < 0.05) in adults ingesting a mineral salt diet, while concentrations of ruminal ammonia, butyrate, and propionate were increased to a significant extent (P < 0.05). Enteric methane emissions were also reduced in heifers ingesting a mineral salt diet, but not to a significant extent (P > 0.05). Moreover, the concentrations of ammonia and volatile fatty acids (VFAs) were not significantly altered in heifers (P > 0.05). Based on these results, we performed high-throughput sequencing to explore the bacterial and archaeal communities of the rumen samples. Succiniclasticum and Prevotella, two propionate-producing bacteria, were predominant in samples of both adults and heifers. At the phylotype level, mineral salt intake led to a significant shift from Succiniclasticum to Prevotella and Prevotellaceae populations in adults. In contrast, reduced abundance of Succiniclasticum and Prevotella phylotypes was observed, with no marked shift in propionate-producing bacteria in heifers. Methanogenic archaea were not significantly abundant between groups, either in adult cows or heifers. The shift of Succiniclasticum to Prevotella and Prevotellaceae in adults suggests a response of microbiota to mineral salt that contributes to higher propionate production, which competes for hydrogen utilized by methanogens. Our data collectively indicate that a mineral salt diet can alter interactions of bacterial taxa that result in enteric methane reduction, and this effect is also influenced in an age-dependent manner.

Protective effect of Bu-Zhong-Yi-Qi decoction, the water extract of Chinese traditional herbal medicine, on 5-fluorouracil-induced intestinal mucositis in mice.

Intestinal mucositis is a serious toxic side effect of 5-fluorouracil (5-FU) treatment. Bu-Zhong-Yi-Qi decoction (BZYQD), a water extract of Chinese traditional herbal medicine, is widely used in chemotherapy in Asia as an alternative treatment to reduce the side effects of chemotherapy. However, the mechanism is unknown. To evaluate its mechanism, we investigated the effect of BZYQD on 5-FU-induced intestinal mucositis in mice, especially with regard to apoptosis in the intestinal mucosal epithelia. In the present study, mice were divided into three groups: control, 5-FU, and 5-FU + BZYQD. Mice in the 5-FU and 5-FU + BZYQD groups were administered 5-FU (100 mg/kg/day, intraperitoneally) for 6 days, and the mice in the latter group were given BZYQD (8 g/kg/day, intragastrically) beginning 4 days before 5-FU and continuing until the termination of the experiment. Loss in body weight and diarrhea during the 5-FU treatment were significantly attenuated by administration of BZYQD. The morphological signs of intestinal damage, including shortened villi height, crypt destruction, apoptosis, and necrosis, in intestinal mucosal epithelia were also reversed, accompanied by reduced neutrophil infiltration, nitrite levels, and inflammatory factors (tumor necrosis factor α and interleukin 1ß) and increased levels of reduced glutathione. These results suggest that BZYQD inhibits 5-FU-induced intestinal mucositis, and this effect may be due to the reduction in apoptosis and necrosis in intestinal mucosal epithelia via the suppression of inflammatory cytokine upregulation. In conclusion, inhibiting cytokine-mediated apoptosis or necrosis can be the molecular mechanism by which BZYQD reduces the gastrointestinal side effects of cancer chemotherapy.