Artemisia argyi (A. argyi) is a Chinese herbal medicine with reported anti-inflammatory effects. In this study, the A. argyi was extracted with water and ethanol, and the concentrations of 35 flavonoids in A. argyi water extract (WE) and ethanol extract (EE) were measured via targeted metabolomics. The antioxidant and anti-inflammatory activities of both WE and EE were firstly explored in vitro via chemical assays and cellular experiment, respectively. Both WE and EE showed significant 1,1-diphenyl-2-picrylhydrazyl (DPPH), 2,2’-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), ·OH, and O2· radical scavenging ability in a dose-dependent manner, and reduced the levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin-22 (IL-22) in lipopolysaccharide (LPS) induced RAW264.7 cell model. In addition, the in vivo anti-colitis activity of both extracts was investigated in dextran sulfate sodium (DSS)-induced colitis mice, and the underlying mechanisms were elucidated by 16S rDNA sequencing and targeted metabolomics. We found that both WE and EE relieved colitis in mice, characterized by decreased disease activity index, increased colon length, improved pathological changes in colon tissue, while EE showed better anti-colitis activity. In addition, both 16S rDNA sequencing and targeted bile acids metabolomics indicated EE modulated gut microbiota and specifically increased the abundance of lithocholic acid (LCA), which might contribute to intestinal barrier function improvement via up-regulating the expression of colonic farnesoid X receptor (FXR). In summary, this study identified the anti-colitis mechanism of A. argyi EE by modulating gut microbiota, facilitating the production of LCA, activating FXR and improving intestinal barrier function.

Ulcerative colitis (UC) is a recurrent inflammatory bowel disease that imposes a severe burden on families and society. In recent years, exploiting the potential of marine bioactive peptides for the treatment of diseases has become a topic of intense research interest. This study revealed the mechanism underlying the protective effect of the dominant polypeptide PKKVV (Pro-Lys-Lys-Val-Val) of Rhopilema esculentum cnidoblasts against DSS-induced UC through a combined analysis of the metagenome and serum metabolome. Specif ically, the polypeptide composition of R. esculentum cnidoblasts was determined by matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF/TOF-MS). Molecular docking showed that the dominant peptide PKKVV could bind better with tumor necrosis factor-α (TNF-α) than the original ligand. Subsequent animal experiments suggested that PKKVV could modulate disorganized gut microorganisms in mice with UC; affect serum metabolites through the arachidonic acid, glycerophospholipid and linoleic acid metabolism pathways; and further alleviate UC symptoms. This study provides a reference for the comprehensive development of marine bioactive substances and nonpharmaceutical treatments for UC.

This study aimed to investigate the protective mechanism of Acaudina leucoprocta peptides (ALPs) in the kidney of type Ⅱ diabetes mice (db/db mice). Serum lipid and glucose indexes were detected in diabetes mice after ALPs treatment. The two-dimensional gel electrophoresis was used to study the kidney protein of diabetic mice. The differential protein screening, GO function annotation, and metabolic pathways were used to determine the protective mechanism of ALPs in the kidney of diabetic mice. The symptoms of db/db mice were alleviated after 10 weeks of treatment with ALPs. The content of TC, TG, and LDL-C in the ALPs group was significantly decreased and the level of HDL-C was increased. After ALPs treatment, the urine glucose and fasting blood glucose of diabetes mice were significantly reduced. The expression of Haptoglobin was up-regulated, it plays a role in anti-inflammatory and immune regulation. And the expression of alpha-2-HS-glycoproteins was down-regulated, then the insulin signal pathway was restored to normal condition, to improve the symptoms of diabetes. This study provided a new strategy that will help treat diabetes.