Ulcerative colitis (UC), a subtype of inflammatory bowel disease, is a chronic gastrointestinal inflammatory disease with unclear etiology and pathophysiology. Herein, we determined the effects of extracellular polysaccharides purified from Aureobasidium pullulans SM-2001 (Polycan) on tight junction protein expression, inflammation, and apoptosis in a dextran sodium sulfate (DSS)-induced acute colitis model. Fifty mice were divided into normal, DSS, DSS + Polycan 250 mg/kg (Polycan 250), DSS + Polycan 500 mg/kg (Polycan 500), and DSS + 5-aminosalicylic acid 100 mg/kg (5-ASA) groups. Their body weights, colon lengths, histological changes in colon tissue, and tight junction function were observed. Results showed that Polycan 250, Polycan 500, and 5-ASA significantly inhibited body weight loss compared with DSS. Similar to 5-ASA, Polycan 500 exhibited preventive effects on colon length shortening and histological changes in colon tissues. Polycan inhibited the DSS-induced decrease in fluorescein isothiocyanate-dextran permeability and myeloperoxidase activity. Moreover, Polycan significantly recovered serum cytokine (e.g., tumor necrosis factor-α, interleukin (IL)-6, and IL-1β) or mRNA expression in colon tissue compared with DSS. Polycan also inhibited apoptosis by reducing caspase-3 activity and the Bcl-2 associated X/B-cell lymphoma 2 (Bcl-2) ratio. Additionally, DSS treatment significantly reduced microbial abundance and diversity, but the administration of Polycan reversed this effect. Collectively, Polycan protected intestinal barrier function and inhibited inflammation and apoptosis in DSS-induced colitis.

Various metabolic diseases caused by a high‐fat diet (HFD) are closely related to gut microbiota dysbiosis and epithelial barrier dysfunction. Polycan, a type of β‐glucan, is effective in treating anti‐obesity and metabolic diseases caused by HFD. However, the effect of Polycan on dysbiosis and epithelial barrier damage is still unknown. In this study, the effects of Polycan on dysbiosis and intestinal barrier damage were investigated using HFD‐induced obese model mice. C57BL/6 mice were fed a HFD for 12 weeks and treated with two different doses of Polycan (250 and 500 mg/kg) orally administered during weeks 9 to 12. Polycan supplementation increased the expression of tight junction genes (zonula occludens‐1, occludin, and claudin‐3) and short‐chain fatty acid (SCFA) content while reducing toxic substances (phenol, p ‐cresol, and skatole). Most significantly, Polycan enriched SCFA‐producing bacteria (i.e., Phocaeicola , Bacteroides , Faecalibaculum , Oscillibacter , Lachnospiraceae, and Muribaculaceae), and decreased the Firmicutes/Bacteroidetes ratio and toxic substances‐producing bacteria (i.e., Olsenella , Clostridium XVIII, and Schaedlerella ). Furthermore, microbial functional capacity prediction of the gut microbiota revealed that Polycan enriched many SCFA‐related KEGG enzymes while toxic substance‐related KEGG enzymes were depleted. These findings indicated that Polycan has the potential to alleviate HFD‐induced intestinal barrier damage by modulating the function and composition of the gut microbiota.

Background and Objectives: The present study investigated the beneficial effects of tart cherry (fruit of Prunus cerasus) concentrated powder (TCcp) on glucocorticoid (GLU)-induced catabolic muscular atrophy in the skeletal muscle of mice. Furthermore, its potential mechanism was also studied. Materials and Methods: Changes in calf thickness, calf muscle weight, calf muscle strength, body weight, gastrocnemius muscle histology, immunohistochemistry, serum creatinine, creatine kinase, lactate dehydrogenase, and antioxidant defense systems were measured. Malondialdehyde, reactive oxygen species, glutathione content, catalase, and superoxide dismutase activities in the gastrocnemius muscle, and muscle-specific mRNA expressions were evaluated. Results: After 24 days, GLU control mice showed muscular atrophy at all criteria of indexes. The muscular atrophy symptoms were significantly inhibited by oral treatment with 250 mg/kg and 500 mg/kg of TCcp through antioxidative and anti-inflammatory modulated expression of genes involved in muscle protein degradation (myostatin, atrogin-1, SIRT1, and MuRF1) and synthesis (A1R, Akt1, TRPV4, and PI3K). Conclusions: This study shows that the TCcp (500 mg/kg and 250 mg/kg) could improve muscular atrophies caused by various etiologies.