Riclin: A novel soluble dietary fiber for promoting gastric health and ameliorating gastric mucosal injury
Focal and diffuse damage to the gastric mucosa contributes to gastric mucosal injury (GMI). Dietary fiber may exert protective effects against GMI; however, its use as a gastrointestinal intervention remains limited. Here, we assessed the potential role of dietary fiber Riclin in GMI. Dietary fiber Riclin exerted a dual effect in enhancing gastric mucosal defense. It modulated microbial-metabolite composition, enhancing biological barriers and reinforcing sustained adhesion to the gastric mucus bicarbonate barrier. Additionally, Riclin enhanced the gastric mucosal immune barrier through the NOD/TLR4/NF-?B pathway. The protective role of Riclin in GMI was revealed by constructing an alcohol-induced murine gastric ulcer model. Our results propose Riclin as a novel dietary fiber with the potential to ameliorate a wide range of gastric disorders characterized by a disrupted gastric mucosal defense and immune dysregulation. In particular, we underscore its potential as a promising dietary fiber for promoting gastric health. Overall design: To investigate the effect of Riclin on the gastric mucosal defense barrier, 20 mice were randomly selected and divided into a control (saline) and Riclin (20 mg/kg) group with continuous gavage administration for 14 d. On the final day, stools were collected from the mice, rapidly frozen in liquid nitrogen, and transferred to a refrigerator (-80 ?) until subsequent testing. To assess the prophylactic effect of Riclin on gastric mucosal injury, ethanol-induced gastric mucosal damage was adopted as a pathological model. Mice were randomly divided into six groups (n = 10/group): the control and model groups were administered saline (0.9%); the omeprazole group was administered omeprazole at a dose of 20 mg/kg; and the experimental groups were administered 5, 10, or 20 mg/kg Riclin. All groups were subjected to continuous gavage administration for 14 d, after which the mice were fasted from food for 24 h before a final gavage treatment. One hour later, all mice, excluding the control group, were administered 0.15 mL/10 mg anhydrous ethanol with 3 h of induction.All mice were euthanized via cervical dislocation after anesthesia. Blood samples were collected from the eye socket, and serum samples were obtained. The stomach of each mouse was cut along the greater curvature and removed. Gastric contents were collected and centrifuged at 1,000 g for 10 min. Hydrogen ion concentration in the stomach content was analyzed using a digital pH meter. Subsequently, the mucus of gastric mucosa was obtained by gently scraping it with a glass slide and weighed on a precision analytical balance. The gastric surface was rinsed with ice-based phosphate-buffered saline (PBS), and surface lesions were observed and scored. A portion of the stomach was stored at -80 °C for biochemical analyses, while the other portion was processed for histopathological, immunohistochemical, and immunofluorescence analyses.