Huicui Liu

Advanced glycation end products (AGEs) are prevalent in thermally processed foods. Long-term intake of AGEs has been linked to intestinal barrier damage, contributing to the development of chronic diseases. Galacto-oligosaccharides (GOS) restored mucus barrier damage induced by dietary AGEs, but the underlying mechanisms remained unclear. This study focused on investigating the effects of GOS on mucin synthesis-related glycosyltransferases, as well as differentiation and apoptosis of goblet cells (GCs) in dietary AGEs-fed C57BL/6 mice. Fecal microbiota transplantation (FMT) was used to probe a possible contribution of the intestinal microbiota. The findings demonstrated that GOS upregulated the mRNA expression of glycosyltransferases (St3gal1 and St3gal3) while inhibiting p-ERK signaling. In addition, no marked changes in mRNA expression of the Wnt, BMP, Notch, and CHOP pathways (which are involved in GC proliferation, differentiation, and apoptosis) were observed following GOS intervention. FMT data suggested the hypothesis that the gut microbiota may participate in mediating changes in St3gal1 and p-ERK/ERK in response to GOS. These findings provided valuable insights into potential interventions for intestinal mucus barrier damage induced by AGEs.

This study employed wild sea buckthorn (Hippophae rhamnoides L.) fruits harvested in Qinghai Province as experimental material. Following compositional analysis of their flavonoids, the antibacterial efficacy and mechanistic pathways of flavonoids in sea buckthorn against Helicobacter pylori (H. pylori) were systematically examined through in vitro and animal model experiments. The results showed that the main flavonoids in sea buckthorn were rutin, quercetin-3-O-glucoside, quercetin, catechin, isorhamnetin, kaempferol-3-O-glucoside, kaempferol and epicatechin. Among them, quercetin, isorhamnetin and kaempferol had strong inhibitory activity against H. pylori. In vitro, sea buckthorn flavonoids inhibited the growth of H. pylori through multiple mechanisms: inducing morphological transformation from rod-shaped to spherical bacteria, promoting cell shrinkage and rupture, disrupting the cell membrane to cause leakage of intracellular macromolecules, increasing membrane permeability, and suppressing urease activity. Sea buckthorn flavonoids exert therapeutic effects on H. pylori-infected mice through multiple mechanisms, including the alleviation of gastric mucosal inflammation via the Nuclear Factor KappaB (NF-κB) signaling pathway, the down-regulation of gastrin-17 (GAS17) to suppress gastric acid production, and the up-regulation of epidermal growth factor (EGF) expression to promote gastric mucosal repair and modulate the composition of gastric microbiota. This study systematically elucidated the anti-H. pylori activity and antibacterial mechanisms of flavonoids derived from sea buckthorn fruits, providing a theoretical basis for the screening of natural antibacterial agents from this plant source.