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Cold is a common source of stress in the alpine areas of northern China. It affects the microbial community, resulting in the invasion of pathogenic microorganisms and intestinal diseases. In recent years, studies have reported that Chinese herbal extracts and their fermentation broth have a significant beneficial effect on gut microbiota. This study aimed to investigate the probiotic effect of a self-designed Chinese herbs complex on the gut microbiota of rats exposed to cold. The rats were treated with intermittent cold exposure and Chinese herbs complex for 14 days, and the gut microbiota composition and other parameters were assayed. The 16s ribosomal DNA high-throughput sequencing and analysis confirmed that the Chinese herbs complex positively improved the gut microbiota. We found that cold exposure could lead to significant changes in the composition of gut microbiota, and affect the intestinal barrier and other physiological functions. The relative abundance of some probiotics in the genus such as Roseburia, Parasutterella, and Elusimicrobium in rats treated with Chinese herbs complex was significantly increased. Serum D-lactic acid (D-LA) and lipopolysaccharide (LPS) were increased in the cold exposure group and decreased in the Chinese herbs complex-treated group. Moreover, the Chinese herbs complex significantly increased the protein expression of occludin. In conclusion, the Chinese herbs complex is effective in restoring the gut microbiota caused by cold exposure, improving the function of the intestinal barrier, and may act as a prebiotic in combatting gut dysbiosis.

Quercetin has a wide range of biological properties that can be used to prevent or decrease particular inflammatory diseases. In this study, we aimed to investigate the gene expression profile and metabolic pathway of the gut microbiota of an antibiotic-treated mouse model administered quercetin. Blood, feces, and intestinal tissue samples were collected and metagenomic sequencing, enzyme-linked immunosorbent assay, and western blot analysis were used to detect variations. The results showed that the quercetin-treated group exhibited increased levels of health beneficial bacterial species, including Faecalibaculum rodentium (103.13%), Enterorhabdus caecimuris (4.13%), Eggerthella lenta (4%), Roseburia hominis (1.33%), and Enterorhabdus mucosicola (1.79%), compared with the model group. These bacterial species were positively related to butyrate, propionate, and intestinal tight junction proteins (zonula occludens-1 and occludin) expression, but negatively related to serum lipopolysaccharide and tumor necrosis factor-α level. In addition, the metabolic pathway analysis showed that dietary quercetin significantly enhanced spliceosomes (111.11%), tight junctions (62.96%), the citrate cycle (10.41%), pyruvate metabolism (6.95%), and lysine biosynthesis (5.06%), but decreasing fatty acid biosynthesis (23.91%) and N-glycan (7.37%) biosynthesis. Furthermore, these metabolic pathway changes were related to relative changes in the abundance of 10 Kyoto Encyclopedia of Genes and Genomes genes (K00244, K00341, K02946, K03737, K01885, k10352, k11717, k10532, K02078, K01191). In conclusion, dietary quercetin increased butyrate-producing bacterial species, and the acetyl-CoA-mediated increased butyrate accelerated carbohydrate, energy metabolism, reduced cell motility and endotoxemia, and increased the gut barrier function, thereby leading to healthy colonic conditions for the host.

BackgroundRemote ischemic conditioning (RIC) is a cardioprotective phenomenon, yet transient ischemia is not a requisite trigger for remote cardioprotection. In fact, RIC is a stimulus compound containing interruption of the blood vessel and tissue compression. In this study, we evaluate the effects of remote tissue compression on infarct size after myocardial infarction and explore its preliminary mechanisms.Methods and ResultsWe used a murine model of myocardial infarction to assess ischemia injury and identified remote conditioning by rhythmic compression on forelimb as a novel cardioprotective intervention. We show that the cardioprotective signal transduction of remote conditioning from the trigger limb to the heart involves the release of adenosine. Our results demonstrate that A2a and A2b receptors are indispensable parts for cardioprotection of remote conditioning, which is linked to its anti-inflammatory properties by the subsequent activation of cAMP/PKA/NF-κB axis.ConclusionOur results establish a new connection between remote tissue compression and cardiovascular diseases, which enhances our cognition about the role of tissue compression on RIC cardioprotection.