D-galacturonic acid ameliorates the intestinal mucosal permeability and inflammation of functional dyspepsia in rats.

BACKGROUND: Functional dyspepsia (FD) is a gastrointestinal disease caused by imbalanced gastrointestinal function. Traditional treatments are deemed to be limited, and new therapeutic drugs are required. New study suggested that duodenal low-grade inflammation and increased intestinal permeability play an important role in the pathogenesis of FD. Previous studies have shown that polysaccharides containing D-galacturonic acid (GA) could modulate intestinal immune activity in vitro and in animal models. However, the ability of GA monomer to improve intestinal mucosal permeability and inflammation in FD has not been clearly elucidated. METHODS: A FD rat model was established using iodoacetamide (IA). FD Rats were administrated different doses of GA. Subsequently, the body weight and behavioral sensitivity of the rats were measured and evaluated; the permeability of the intestinal barrier was measured by determining D-lactose, lactulose/mannitol ratio (LMR), and permeability-related genes [desmocollin-2 (DSC2), TJP1, and OCLN] in FD rats. Also, inflammatory cells [cluster of differentiation (CD)3+ cells and mast cells] were assessed by immunohistochemistry, and the levels of immune-related factors, such as the Toll-like receptor-nuclear factor kappa B (TLR/NF-κB) pathway, were monitored by reverse transcription quantitative polymerase chain reaction (RT-qPCR) or western blot assays. RESULTS: Our results suggested that GA could markedly increase the body weight and attenuate the behavioral sensitivity of FD rats. Moreover, GA also has an obvious ameliorating effect on the intestinal mucosal permeability and inflammatory response of FD rats. Furthermore, we found that GA could markedly downregulate TLR2, TLR4, and NF-κB in FD rats. CONCLUSIONS: These findings indicate that GA could significantly attenuate the intestinal mucosal permeability and inflammation FD rats. The effect of GA was partially mediated by the TLR/NF-κB signaling pathway.

A case report of a post-polypectomy syndrome with severe sepsis and organ dysfunction.

Post-polypectomy syndrome (PPS) results from electrocoagulation injury to the bowel wall that induces a transmural burn and localized peritonitis. It has a good prognosis; however, there are exceptions when complications are observed. We here report a case of a 50-year-old man who developed lumbosacral pain and high fever with chills four days after colonoscopy, during which polypectomy was performed by endoscopic mucosal resection (EMR) and argon plasma coagulation (APC). Both the plain abdominal film and abdominal CT scan showed no free air, and lumbar CT showed no apparent lesions, which satisfied the diagnosis of PPS. However, the patient was in a critical condition as he developed septic shock caused by bacteremia. Following active treatment, the patient's condition rapidly improved. Therefore, we suggest that clinicians should consider the severity of PPS with sepsis and colon transmural burn. Patients with a diagnosis of PPS should be admitted to the hospital for observation and treatment to avoid adverse consequences.