Ulcerative colitis (UC) is a disease that is difficult to treat and has been associated with high rates of recurrence. Moreover, the current medications for UC induce serious side effects following prolonged use. Ganjiang Huangqin Huanglian Renshen Decoction (GJHQHLRSD), has been traditionally used to treat UC. However, its protective mechanisms have not been fully studied. In this study the mechanisms by which GJHQHLRSD treats UC was investigated. The GJHQHLRSD and GJHQHLRSD drug-containing serum (GJHQHLRSD-DS) were characterized using LC-MS/MS. The therapeutic effect of GJHQHLRSD on dextran sodium sulfate (DSS)-induced UC was explored by assessing various parameters including intestinal flora 16S rRNA, intestinal barrier function, oxidative stress (OS) response, inflammatory cytokines, colonic histopathological injury, colon length, disease activity index (DAI) and body weight. Treatment with GJHQHLRSD increased body weight, ameliorated colon length shortening and edema, reduced the DAI score, improved the pathological injury, down-regulated the levels of IL-1β, IL-6, IL-8, TNF-α, LPS, LDH, TLR4, and NLRP3, and up-regulated the ZO-1 and Occludin levels in UC mice. It also decreased intestinal oxidative stress in UC mice and improved mitogenic activity by modulating mitochondrial ultrastructure as well as the expression level of PINK1, LC3-II/Ⅰ, Beclin-1, p62, and Parkin proteins. In addition, we found that the effects of GJHQHLRSD on UC mice were inhibited by 3-MA.GJHQHLRSD treatment reduced the imbalance of intestinal flora in UC mice, by regulating the inflammation and oxidative stress. These findings suggested that GJHQHLRSD effectively attenuated inflammatory responses, inhibited the TLR4/NF-κB/NLRP3 signalling, oxidative stress, and modulated the gut microbiota, and alleviated the DSS-induced UC symptoms, making it a promising and innovative therapeutic option for the treatment of UC.

Mitochondria are important organelles that regulate cellular energy and biosynthesis, as well as maintain the body’s response to environmental stress. Their dynamics and autophagy influence occurrence of cellular function, particularly under stressful conditions. They can generate reactive oxygen species (ROS) which is a major contributor to inflammatory diseases such as ulcerative colitis (UC). In this review, we discuss the key effects of mitochondrial dynamics and mitophagy on the pathogenesis of UC, with a particular focus on the cellular energy metabolism, oxidative stress, apoptosis, and immunoinflammatory activities. The therapeutic efficacy of existing drugs and phytochemicals targeting the mitochondrial pathway are discussed to reveal important insights for developing therapeutic strategies for treating UC. In addition, new molecular checkpoints with therapeutic potential are identified. We show that the integration of mitochondrial biology with the clinical aspects of UC may generate ideas for enhancing the clinical management of UC.

Background. Ulcerative colitis (UC), a chronic and nonspecific inflammatory bowel disease, seriously affects the quality of patients life. Han Re Bing Yong Fa (treating diseases with both cool- and warm-natured herbs) is a classical therapeutic principle of traditional Chinese medicine (TCM), which is often used to treat chronic diseases, including UC. The Gan Jiang-Huang Qin-Huang Lian-Ren Shen decoction (GJHQHLRSD), a representative of Han Re Bing Yong Fa, is effective in alleviating inflammatory symptoms in UC. However, the pharmacological mechanism underlying its anti-inflammatory effect remains unclear. Methods. A network pharmacology strategy, including the construction and analysis of the drugdisease network, was used to explore the complex mechanism of GJHQHLRSD treatment of UC. In addition, molecular docking technology was used to preliminarily examine the binding ability of the potential active components and core therapeutic targets of GJHQHLRSD. Results. The network pharmacology results revealed 140 targets of GJHQHLRSD which are involved in UC. The PPI network analysis identified seven target genes: BCL2L1, NR3C1, ALOX5, S1PR5, NR1I2, CYP2D6, and LPAR6. The molecular docking results revealed that the following displayed strongest combined effects: EGFR with kaempferol, ERK1 with worenine, STAT3 with Palmidin A, BCL2L1 with diop and VEGFA with ginsenoside Rg3. The KEGG and gene ontology enrichment analyses results indicated that GJHQHLRSD functions by regulating the EGFR signaling pathway in UC treatment. Other effective biological processes involved in UC treatment included cancer-related as well as inflammation and viral infection signaling pathways, such as the MicroRNAs in cancer, TNF signaling pathway, and JAK-STAT signaling pathway. Conclusions. This study reflects the multicomponent, multitarget, and multipathway characteristics of the action mechanism of GJHQHLRSD in treating UC. Furthermore, it helps better understand the TCM therapeutic principle of Han Re Bing Yong Fa and explore novel candidate drug targets for UC treatment.

Background: Ulcerative colitis (UC) is a chronic inflammatory bowel disease affecting millions worldwide. Tofacitinib, an inhibitor of Janus kinase (JAK), has shown considerable potential as an effective treatment option for individuals suffering from moderate to severe UC, aiming to mitigate the risk of colectomy, hospitalization, and disease exacerbation.Methods: We conducted a comprehensive literature review from 2012 to 2024 to assess the study landscape of Tofacitinib in UC. Employing the Web of Science Core Collection database (WOSCC) and the bibliometric tool CiteSpace, we performed an bibliometric analysis to delineate disciplinary evolution and identify research hotspots within the UC Tofacitinib domain.Results: Our analysis extracted 406 UC Tofacitinib-related articles from WOSCC, indicating a growing body of literature. The United States and Europe are at the forefront of research maturity, with a significant contribution to the field. Here we show that multidisciplinary research is burgeoning, which is crucial for the advancement of UC Tofacitinib studies. We identified 13 highly cited documents and 10 co-cited documents, highlighting Tofacitinib’s prominence as a small molecule agent. Keyword analysis revealed that the intestinal barrier, clinical response, remission rate, and safety are the central themes of current research.Conclusion: By applying bibliometrics, citation analysis, and knowledge mapping, this study provides a snapshot of the current state and trajectory of Tofacitinib research in UC. We have elucidated the knowledge lineage in this field, offering insights that can inform both ongoing and future research endeavors. Our findings underscore the importance of multidisciplinary collaboration in advancing UC therapeutic strategies.

Inflammatory bowel disease (IBD) and Alzheimer’s disease (AD) are two chronic conditions previously considered pathologically unrelated. However, accumulating epidemiological evidence suggests that patients with IBD may have an elevated risk. This review systematically analyzes the mechanistic links between IBD and AD, emphasizing the roles of gut microbiota dysbiosis, systemic and neuroinflammation, and glymphatic dysfunction. We propose a putative conceptual framework incorporating the ‘gut–glymphatic axis’ as a potential conduit through which IBD-associated microbial and immune perturbations may influence AD pathology. Key pathways include short-chain fatty acids, tryptophan metabolites, trimethylamine N-oxide, and bile acids, all of which modulate neuroinflammation and amyloid-β clearance. Additionally, circadian disruption and impaired aquaporin-4 polarity in the glymphatic system may represent novel links between intestinal inflammation and neurodegenerative changes. Preclinical animal models suggest that colitis exacerbates AD-like pathology via NLRP3 inflammasome activation, neutrophil infiltration, and microglial dysfunction. Natural bioactive compounds—such as ginsenosides, curcumin, baicalin, berberine, and magnolol—show dual therapeutic potential in both IBD and AD by targeting shared inflammatory and microbiota pathways. However, validated comorbidity models and clinical trials are lacking. This review provides a scientifically grounded basis for future mechanistic studies and integrated interventions for IBD–AD comorbidity.