ATX has protective effects on intestinal mucosal dysfunction in Cy-induced immunodeficient mice.

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ScopeCachexia, which is often marked by skeletal muscular atrophy, is one of the leading causes of death in cancer patients. Astaxanthin, a carotenoid obtained from marine organisms that can aid in the prevention and treatment of a variety of disorders. In this study, to assess whether astaxanthin ameliorates weight loss and skeletal muscle atrophy in sorafenib‐treated hepatocellular carcinoma mice is aimed.Methods and resultsH22 mice are treated with 30 mg kg−1 day−1 of sorafenib and 60 mg kg−1 day−1 of astaxanthin by gavage lasted for 18 days. Sorafenib does not delay skeletal muscle atrophy and weight loss, although it does not reduce tumor burden. Astaxanthin dramatically delays weight loss and skeletal muscle atrophy in sorafenib‐treating mice, without affecting the food intake. Astaxanthin inhibits the tumor glycolysis, slows down gluconeogenesis, and improves insulin resistance in tumor‐bearing mice. Astaxanthin increases glucose competition in skeletal muscle by targeting the PI3K/Akt/GLUT4 signaling pathway, and enhances glucose utilization efficiency in skeletal muscle, thereby slowing skeletal muscle atrophy.ConclusionThe findings show the significant potential of astaxanthin as nutritional supplements for cancer patients, as well as the notion that nutritional interventions should be implemented at the initiation of cancer treatment, as instead of waiting until cachexia sets in.

Mannuronate oligosaccharide (MOS) is α-D-mannuronic acid polymer with 1,4-glycosidic linkages that possesses beneficial biological properties. The aim of this study was to investigate the hypouricemic effect of MOS in hyperuricemic mice and demonstrate the possible protective mechanisms involved. In this research, 200 mg/kg/day of MOS was orally administered to hyperuricemic mice for four weeks. The results showed that the MOS treatment significantly reduced the serum uric acid (SUA) level from 176.4 ± 7.9 μmol/L to 135.7 ± 10.9 μmol/L (p < 0.05). MOS alleviated the inflammatory response in the kidney. Moreover, MOS promoted uric acid excretion by regulating the protein levels of renal GLUT9, URAT1 and intestinal GLUT9, ABCG2. MOS modulated the gut microbiota in hyperuricemic mice and decreased the levels of Tyzzerella. In addition, research using antibiotic-induced pseudo-sterile mice demonstrated that the gut microbiota played a crucial role in reducing elevated serum uric acid of MOS in mice. In conclusion, MOS may be a potential candidate for alleviating HUA symptoms and regulating gut microbiota.

Summary This study investigated the degradation effect of curcumin‐mediated photodynamic technology (PDT) on polycyclic aromatic hydrocarbons (PAHs) in oysters, and evaluated the safety of PDT‐treated oysters through acute and subacute toxicity experiments. The results demonstrated that curcumin‐mediated PDT could effectively degrade multi‐component PAHs in oysters, the maximum removal efficiency could reach 80.20% (10 μmol L−1 curcumin concentration and 54 J cm−2 light energy density). Acute toxicity experiment revealed PDT‐treated oysters did not cause any mortality and adverse symptoms in mice at an oral dose of 40 g kg−1 BW. Besides, after being treated at the dose of 10 g kg−1 BW for 28 days, the rats showed no obvious abnormal change in the indicators including the body weight, food utilisation, urology, haematology, serum biochemistry, organ index and histopathology. These findings show curcumin‐mediated PDT is a potentially efficacious method to degrade PAHs in oysters, and PDT‐treated oysters have high edible safety.