Probiotics for the treatment of ulcerative colitis: a review of experimental research from 2018 to 2022.

Ulcerative colitis (UC) has become a worldwide public health problem, and the prevalence of the disease among children has been increasing. The pathogenesis of UC has not been elucidated, but dysbiosis of the gut microbiota is considered the main cause of chronic intestinal inflammation. This review focuses on the therapeutic effects of probiotics on UC and the potential mechanisms involved. In animal studies, probiotics have been shown to alleviate symptoms of UC, including weight loss, diarrhea, blood in the stool, and a shortened colon length, while also restoring intestinal microecological homeostasis, improving gut barrier function, modulating the intestinal immune response, and attenuating intestinal inflammation, thereby providing theoretical support for the development of probiotic-based microbial products as an adjunctive therapy for UC. However, the efficacy of probiotics is influenced by factors such as the bacterial strain, dose, and form. Hence, the mechanisms of action need to be investigated further. Relevant clinical trials are currently lacking, so the extension of animal experimental findings to clinical application requires a longer period of consideration for validation.

Pretreatment with Bifidobacterium longum BAA2573 ameliorates dextran sulfate sodium (DSS)-induced colitis by modulating gut microbiota.

Objectives: Inflammatory bowel disease (IBD) is a chronic lifelong inflammatory disease. Probiotics such as Bifidobacterium longum are considered to be beneficial to the recovery of intestinal inflammation by interaction with gut microbiota. Our goals were to define the effect of the exclusive use of BAA2573 on dextran sulfate sodium (DSS)-induced colitis, including improvement of symptoms, alleviation of histopathological damage, and modulation of gut microbiota. Methods: In the present study, we pretreated C57BL/6J mice with Bifidobacterium longum BAA2573, one of the main components in an over-the-counter (OTC) probiotic mixture BIFOTO capsule, before modeling with DSS. 16S rDNA sequencing and liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based non-targeted metabolomic profiling were performed with the collected feces. Results: We found that pretreatment of Bifidobacterium longum BAA2573 given by gavage significantly improved symptoms and histopathological damage in DSS-induced colitis mice. After the BAA2573 intervention, 57 genera and 39 metabolites were significantly altered. Pathway enrichment analysis demonstrated that starch and sucrose metabolism, vitamin B6 metabolism, and sphingolipid metabolism may contribute to ameliorating colitis. Moreover, we revealed that the gut microbiome and metabolites were interrelated in the BAA2573 intervention group, while Alistipes was the core genus. Conclusion: Our study demonstrates the impact of BAA2573 on the gut microbiota and reveals a possible novel adjuvant therapy for IBD patients.

Curcumin-induced histone acetylation inhibition improves stress-induced gastric ulcer disease in rats.

Curcumin is known to possess anti­inflammatory properties. Despite the fact that curcumin is known to be a strong inhibitor of H+, K+­ATPase activity, the mechanism underlying the curcumin­induced inhibition of the transcription of the H+, K+­ATPase α subunit in gastric mucosal parietal cells remains unclear. The present study investigated the possible mechanism by which curcumin inhibits stomach H+, K+­ATPase activity during the acute phase of gastric ulcer disease. A rat model of stress­induced gastric ulcers was produced, in which the anti­ulcer effects of curcumin were examined. Curcumin­induced inhibition of the H+, K+­ATPase promoter via histone acetylation, was verified using a chromatin immunoprecipitation assay. The results showed that curcumin improved stress­induced gastric ulcer disease in rats, as demonstrated by increased pH values and reduced gastric mucosal hemorrhage and ulcer index. These effects were accompanied by a significant reduction in the level of histone H3 acetylation at the site of the H+, K+­ATPase promoter and in the expression of the gastric H+,K+­ATPase α subunit gene and protein. In conclusion, curcumin downregulated the acetylation of histone H3 at the site of the H+, K+­ATPase promoter gene, thereby inhibiting the transcription and expression of the H+, K+­ATPase gene. Curcumin was shown to have a preventive and therapeutic effect in gastric ulcer disease.