porphyran and Disease-Models--Animal

Porphyran is known to inhibit immune cell function. Previously, porphyran was shown to prevent lipopolysaccharide-induced sepsis in mice. However, studies on the inhibitory effects of porphyran during colitis are currently lacking. In this study, we evaluated the effects of Pyropia yezoensis-derived porphyran on dextran sodium sulfate (DSS)-induced acute and chronic colitis. The oral or intraperitoneal administration of porphyran inhibited the progression of DSS-induced colitis in mice, with the former also preventing immune cell infiltration in the colon. The levels of intracellular interferon-γ and interleukin-17 in T cells decreased when porphyran was administered orally. Porphyran inhibited T cell activation by suppressing dendritic cells (DCs) and macrophages. Porphyran prevented pathogen-associated molecular pattern and damage-associated molecular pattern-dependent DC and macrophage activation. Finally, porphyran attenuated chronic colitis caused via the long-term administration of DSS. These findings indicate that the oral administration of porphyran can inhibit DSS-induced colitis by suppressing DC and macrophage activation.

Topics: Animals; Colitis; Colon; Dendritic Cells; Dextran Sulfate; Disease Models, Animal; Mice; Mice, Inbred C57BL; Rhodophyta; Sepharose

The pharmacological values of marine algal polysaccharides on gut health are being recognized in recent research. However, the protective effect of degraded polysaccharides from

Topics: Animals; Colitis; Colitis, Ulcerative; Colon; Dextran Sulfate; Disease Models, Animal; Galactose; Gastrointestinal Microbiome; Mice; Mice, Inbred C57BL; Phylogeny; Polysaccharides; RNA, Ribosomal, 16S

Porphyran and its derivatives possess a variety of biological activities, such as ameliorations of oxidative stress, inflammation, hyperlipemia, and immune deficiencies. In this study, we evaluated the potential efficacy of porphyran-derived oligosaccharides from Porphyra yezoensis (PYOs) in alleviating nonalcoholic fatty liver disease (NAFLD) and preliminarily clarified the underlying mechanism. NAFLD was induced by a high-fat diet for six months in C57BL/6J mice, followed by treatment with PYOs (100 or 300 mg/kg/d) for another six weeks. We found that PYOs reduced hepatic oxidative stress in mice with NAFLD, which plays a critical role in the occurrence and development of NAFLD. In addition, PYOs could markedly decrease lipid accumulation in liver by activating the IRS-1/AKT/GSK-3β signaling pathway and the AMPK signaling pathway in mice with NAFLD. PYOs also apparently relieved the hepatic fibrosis induced by oxidative stress via downregulation of TGF-β and its related proteins, so that liver injury was markedly alleviated. Furthermore, PYOs treatment relieved cecal microbiota dysbiosis (such as increasing the relative abundance of Akkermansia, while decreasing the Helicobacter abundance), which could alleviate oxidative stress, inflammation, and lipid metabolism, and protect the liver to a certain degree. In summary, PYOs treatment remarkably improved NAFLD via a specific molecular mechanism and reshaped the cecal microbiota.

Topics: Animals; Cecum; Disease Models, Animal; Dysbiosis; Gastrointestinal Microbiome; Lipid Metabolism; Male; Mice; Mice, Inbred C57BL; Non-alcoholic Fatty Liver Disease; Oligosaccharides; Oxidative Stress; Sepharose; Signal Transduction

Topics: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Animals; Apoptosis; Behavior, Animal; Brain; Disease Models, Animal; Dopamine; Dopaminergic Neurons; Humans; Male; Mice; Mice, Inbred C57BL; MPTP Poisoning; Neuroprotective Agents; Phosphatidylinositol 3-Kinases; Porphyra; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-bcl-2; Sepharose; Signal Transduction

Porphyran (POR) from the red alga Porphyra yezoensis is a water soluble dietary fiber. In this study, we investigated the effect of dietary POR on glucose metabolism in KK-Ay mice (a model for type 2 diabetes). Mice were divided into 4 groups and fed a diet containing 5% cellulose (control), POR, POR Arg or POR K. After 3 wk of feeding, plasma insulin levels and the calculated homeostasis model assessment-insulin resistance (HOMA-IR) index were significantly lower in the POR group than in the control group. Compared with the control group, plasma adiponectin levels were significantly increased in the POR, POR Arg and POR K groups. These results suggest that dietary POR should improve glucose metabolism in diabetes via up-regulation of adiponectin levels. In addition, the amount of propionic acid in the cecum of the POR group was significantly higher than in the control group and the profile of bacterial flora was changed by dietary POR. In the cecum of the POR, POR Arg and POR K groups, Bacteroides was significantly increased and Clostridium coccoides was significantly decreased compared with in the control group. The effects of dietary POR on the hindgut environment might contribute to the improvement of glucose metabolism.

Topics: Adiponectin; Animals; Cecum; Cholesterol; Diabetes Mellitus, Type 2; Dietary Fiber; Disease Models, Animal; Fatty Acids, Nonesterified; Glucose; Insulin; Insulin Resistance; Male; Mice; Porphyra; Real-Time Polymerase Chain Reaction; RNA, Bacterial; Sepharose; Triglycerides