Aamir Saleem

Background: Hyperuricemia (HU) results from excessive uric acid (UA) production/impaired excretion and is associated with gout and renal dysfunction. Gut microbiota dysbiosis may impair intestinal UA excretion, disrupt the gut barrier, and promote inflammation. Traditional Chinese medicine (TCM), with multitarget and microbiota-modulating effects, may offer a therapeutic strategy for HU. In this study, the rhizome of Phragmites communis, a TCM used for clearing heat and promoting diuresis, was investigated. Specifically, we evaluated whether P. communis could alleviate HU by suppressing xanthine oxidase (XOD) and modulating urate transporter expression, thereby reducing UA production while promoting its excretion. Method: The effects of a crude extract of P. communis were investigated with in vitro and in vivo models using molecular, 16S rRNA sequencing, and metabolomic analyses. Results: P. communis significantly decreased serum uric acid (SUA) levels by inhibiting XOD and improving renal and intestinal urate excretion, accompanied by decreased renal and increased intestinal solute carrier family 2 member 9 (SLC2A9) and enhanced ATP-binding cassette subfamily G member 2 (ABCG2) expression, restored gut barrier integrity, and suppressed inflammation. Microbiota analysis revealed enrichment of Ligilactobacillus, Prevotella, and Dubosiella. Fecal metabolomics identified hippuric acid (HA), which correlated with Ligilactobacillus abundance. In vitro, HA enhanced ABCG2, PDZ domain-containing 1 (PDZK1), and SLC2A9 expression. Molecular docking identified feruloylquinic acid (FAQ) as the favorable XOD inhibitor. Conclusions: P. communis exerts anti-hyperuricemic effects by inhibiting UA biosynthesis, promoting UA excretion, modulating gut microbiota, restoring gut barrier integrity, and suppressing inflammation, highlighting its potential as a TCM-based therapeutic intervention for HU.

Chronic atrophic gastritis (CAG) is a pivotal precancerous condition in gastric carcinogenesis, with progression typically following the classic Correa cascade. Although Helicobacter pylori (H. pylori) infection is widely recognized as the principal etiological factor, the persistence of gastric cancer (GC) risk in a subset of patients after successful eradication suggests that gastric microbiota dysbiosis may also contribute to CAG progression. In recent years, high-throughput sequencing technologies have revealed distinct microbial restructuring in patients with CAG, characterized by decreased microbial diversity, depletion of commensal taxa, and enrichment of opportunistic pathogens. These compositional changes are accompanied by metabolic dysfunction, activation of inflammatory signaling pathways, and disruption of immune homeostasis, which may contribute to a microenvironment permissive for precancerous transformation of the gastric mucosa. Probiotics and related microbiome-based therapeutics, including prebiotics, synbiotics, and postbiotics, have emerged as promising adjunctive strategies for H. pylori eradication and disease management. Their beneficial effects are mediated through multiple mechanisms, including remodeling of the microbial community, inhibition of pathogen colonization, modulation of host immune responses, and restoration of mucosal barrier integrity. However, whether these interventions can reverse established atrophic or metaplastic lesions remains unclear. In addition, how strain specificity, dose dependency, and interindividual heterogeneity influence clinical efficacy has yet to be fully elucidated. In this review, we summarize the compositional and functional features of gastric microbiota dysbiosis in patients with CAG, as well as the mechanisms and clinical applications of microbiome-based interventions. We further highlight current limitations in the field and discuss future directions for precision microecological therapies integrating multi-omics approaches, engineered probiotics, and artificial intelligence. These advances may provide a theoretical framework and practical guidance for the diagnosis and management of CAG and the prevention of GC.