Dysbiosis of the gut microbiota is emerging as a pivotal factor in the pathogenesis of colorectal cancer (CRC). Ginsenoside Rh4 (Rh4) is an active compound isolated from ginseng with beneficial effects in modulating intestinal inflammation and gut microbiota dysbiosis, but how Rh4 regulates the gut microbiota to alleviate CRC remains underexplored. We investigated the impact of Rh4 on CRC and the mechanism of its action in inhibiting CRC via modulation of gut microbiota. We used the AOM/DSS model and employed transcriptomics, genomics and metabolomics techniques to explore the inhibitory impact of Rh4 on CRC. Furthermore, we employed experiments involving antibiotic treatment and fecal microbiota transplantation (FMT) to investigate the role of the gut microbiota. Finally, we elucidated the pivotal role of key functional bacteria and metabolites regulated by Rh4 in CRC. Our research findings indicated that Rh4 repaired intestinal barrier damage caused by CRC, alleviated intestinal inflammation, and inhibited the development of CRC. Additionally, Rh4 inhibited CRC in a gut microbiota-dependent manner. Rh4 increased the diversity of gut microbiota, enriched the probiotic Akkermansia muciniphila (A. muciniphila), and alleviated gut microbiota dysbiosis caused by CRC. Subsequently, Rh4 regulated A. muciniphila-mediated bile acid metabolism. A. muciniphila promoted the production of UDCA by enhancing the activity of 7α-hydroxysteroid dehydrogenase (7α-HSDH). UDCA further activated FXR, modulated the TLR4-NF-κB signaling pathway, thus inhibiting the development of CRC. Our results confirm that Rh4 inhibits CRC in a gut microbiota-dependent manner by modulating gut microbiota-mediated bile acid metabolism and promoting the production of UDCA, which further activates the FXR receptor and regulates the TLR4-NF-κB signaling pathway. Our results confirm that Rh4 has the potential to be used as a modulator of gut microbiota for preventing and treatment of CRC.

The aim of this research was to prepare a novel sponge-like porous hydrogel scaffold based on human-like collagen (HLC) that could be applied in cartilage tissue regeneration. In this study, bovine serum albumin (BSA) was used as a porogen to prepare the porous hydrogel, which had not been previously reported. Glutamine transaminase (TGase) was used as the cross-linker of the hydrogel, because it could catalyze the cross-linking of BSA. During the crosslinking process, BSA and HLC were mixed together, which affected the cross-linking of HLC. When the cross-linking was completed, the non-crosslinked section formed pores. The microstructure, porosity, swelling properties, and compressive properties of the hydrogel were studied. The results showed that the pore size of the hydrogel was between 100 and 300 μm, the porosity reached up to 93.43%, and the hydrogel had rapid water absorption and suitable mechanical properties. Finally, we applied the hydrogel to cartilage tissue engineering through in vitro and in vivo research. The in vitro cell experiments suggested that the hydrogel could promote the proliferation and adhesion of chondrocytes, and in vivo transplantation of the hydrogel could enhance the repair of cartilage. In general, the hydrogel is promising as a tissue engineering scaffold for cartilage.

Hydrogel-based wound dressings provide a cooling sensation, a moist environment, and act as a barrier to microbes for wounds. In this study, a series of soft, flexible, porous non-stick hydrogel dressings were prepared through the simple repeated freeze-thawing of a poly(vinyl alcohol), human-like collagen (or and carboxymethyl chitosan) mixed solution rather than chemical cross-linking and Tween80 was added as pore-forming agent for cutaneous wound healing. Some of their physical and chemical properties were characterized. Interestingly, hydrogel PVA-HLC-T80 and PVA-HLC-CS-T80 presented excellent swelling ratios, bacterial barrier activity, moisture vapor permeability, hemostasis activity and biocompatibility. Furthermore, in vivo evaluation of the healing capacity of these two hydrogels was checked by creating a full-thickness wound defect (1.3 cm × 1.3 cm) in rabbit. Macroscopic observation and subsequent hematoxylin eosin staining (H&E) staining and transmission electron microscopy (TEM) analysis at regular time intervals for 18 days revealed that the hydrogels significantly enhanced wound healing by reducing inflammation, promoting granulation tissue formation, collagen deposition and accelerating re-epithelialization. Taken together, the obtained data strongly encourage the use of these multifunctional hydrogels for skin wound dressings.

Non-alcoholic fatty liver disease (NAFLD) is a series of disorders of liver metabolism caused by the accumulation of lipids in the liver, which is considered the main cause of hepatocellular carcinoma. Our previous study demonstrated the promising efficacy of ginsenoside Rh4 in improving the intestinal tract and its related metabolites. Meanwhile, many studies in the literature have investigated the gut microbiota and its metabolites, such as bile acids (BAs) and short-chain fatty acids (SCFAs), which play a key role in the pathogenesis of NAFLD. Therefore, this study focused on whether Rh4 could achieve therapeutic effects on NAFLD through the gut–liver axis. The results showed that Rh4 exhibited sound therapeutic effects on the NAFLD model induced by the Western diet and CCl₄ in mice. In the liver, the degrees of hepatic steatosis, lobular inflammation levels, and bile acid in the liver tissue were improved after Rh4 treatment. At the same time, Rh4 treatment significantly increased the levels of intestinal SCFAs and BAs, and these changes were accompanied by the complementary diversity and composition of intestinal flora. In addition, correlation analysis showed that Rh4 affected the expression of proteins involved in the farnesoid X receptor (FXR) signaling pathway in the liver and intestine, which modulates hepatic lipid metabolism, inflammation, and proteins related to bile acid regulation. In conclusion, our study provides a valuable insight into how Rh4 targets the gut–liver axis for the development of NAFLD, which indicates that Rh4 may be a promising candidate for the clinical therapy of NAFLD.