ETHNOPHARMACOLOGICAL RELEVANCE:The modified Zuojin formula (SQQT) has been clinically prescribed for gastric metaplasia (GM) for several decades in China. The therapeutic efficacy of SQQT and potential mechanisms have been demonstrated in our previous studies. This research will further investigate its mechanism in the immune microenvironment. AIM OF THE STUDY:We aimed to determine the influence of SQQT on the ILC2-mediated JAK-2/STAT5/c-Myc pathway during GM. METHODS:The mechanism of GM in patients was measured through single-cell RNA sequencing. The constituents of SQQT have been examined before. The role of SQQT targets JAK-2/STAT5/c-Myc pathway was verified by network pharmacology and molecular docking. The model of GM was induced by tamoxifen (5 mg/20 g), CD90.2 protein (200 μg) or SQQT (1.69, 3.38, 6.76 g/kg) was given to treat GM mice. The SQQT mechanism was confirmed by both in vitro and in vivo studies. Histological analysis, serum cytokines, and protein levels were assessed. RESULTS:Single-cell RNA sequencing analysis indicated that ILC2 increased in the GM patients, the goblet cells in GM were probably transferred from endocrine cells. Compounds in SQQT are related to cell proliferation and can bind to the JAK-2/STAT5/c-Myc pathway proteins. The main components of SQQT, can spontaneously bind to the JAK-2 protein in 9 sites. Tamoxifen caused body weight decrease, spleen weight increase, stomach injury, ILC2 increase, and cytokines increase in the GM group. After examining the cytokines, IL-5 was the only one significantly increased in the GM group. CD90.2 and SQQT can alleviate histological changes of the stomach corpus, inflammation cytokines, and other GM-related indicators. Moreover, cell proliferation and JAK-2 pathway markers were depressed in GM mice. Besides, SQQT protects GES-1 cells from IL-5 injury related to upregulating JAK-2/STAT5/c-Myc proteins in 24h, 48h and 72h. CONCLUSION:The mechanism of SQQT protected the stomach from metaplasia associated to ILC2 activation and the subsequent cell proliferation through IL-5/JAK-2/STAT5/c-Myc pathway.

ObjectiveNon-erosive reflux disease (NERD) is a prevalent gastrointestinal disorder with complex pathophysiology. Recent evidence suggests a potential role of gut microbiota in its development. This study aimed to characterize the gut microbiota in patients with NERD, and to explore microbial biomarkers for disease differentiation.MethodsWe enrolled 40 patients with NERD, along with 18 healthy controls (HCs). Fecal samples were collected and analyzed using 16S ribosomal RNA (rRNA) gene sequencing. Gut microbial diversity and composition, linear discriminant analysis effect size (LEfSe), and receiver operating characteristic (ROC) curves were evaluated.ResultsThe microbial structure and composition of NERD patients were distinct from those of HCs. Alpha diversity was significantly lower in NERD patients than in controls (p < 0.01). At the phylum level, Actinobacteriota was increased, while Bacteroidota and Proteobacteria were decreased in NERD patients. At the genus level, Faecalibacterium and Bacteroides were decreased, whereas Streptococcus, Blautia, Bifidobacterium, and Enterococcus were enriched in NERD patients. Additionally, LEfSe was developed to identify several bacterial genera that can differentiate patients with NERD from those HCs. Furthermore, the area under the curve (AUC) value of Streptococcus for distinguishing NERD from HCs was 0.9333, indicating exceptionally high diagnostic power.ConclusionThis study identified microbiota dysbiosis of gut microbiota in NERD patients. Streptococcus showed extremely high diagnostic efficacy, which can be used as a microbial biomarker, and may serve as potential therapeutic target for NERD.

Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease characterized by mucosal inflammation and epithelial barrier disruption. The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, the principal cytosolic DNA-sensing axis, has emerged as a critical node in UC pathogenesis. This review elucidates the cGAS/STING signaling network in UC, from its upstream activation triggered by exogenous stimuli and leaked endogenous DNA to its downstream effects. We discuss how this pathway modulates distinct lines of intestinal defense, including the mechanical, chemical, and immunological barriers, while integrating its bidirectional crosstalk with the microbial barrier. Rather than exerting purely detrimental effects, cGAS/STING functions as a double-edged sword that coordinates both barrier homeostasis and inflammatory pathogenesis. Crucially, we summarize current pharmacological interventions, highlighting synthetic small molecules and bioactive natural products that target and modulate this axis to restore intestinal equilibrium. This framework provides a theoretical foundation for future precision therapies in UC.

IntroductionUlcerative colitis (UC) is being increasingly connected to the pathogen Veillonella parvula (V. parvula). Modified Gegen Qinlian Decoction (MGQD), a traditional Chinese medicine therapy, is used to treat UC. However, the underlying mechanism by which V. parvula exacerbates UC and whether MGQD can alleviate it is unknown.MethodsMGQD therapy was tested on pathogen-free and pseudo-germ-free mice infected with V. parvula. Colitis severity was determined by disease activity index, colon length, and histology. Transmission electron microscopy, Western blot, immunofluorescence, and immunohistochemistry were used to assess the integrity of the intestinal mucosal barrier. In vitro, mouse colonic organoids were utilized to examine the effects of baicalin and puerarin on inflammation-induced downregulation of Muc2 and ZO-1.ResultsMGQD therapy dramatically reduced the severity of colitis in both mouse models. MGQD restored the integrity of the mucus and mechanical barriers. Furthermore, baicalin and puerarin reduced inflammation-induced downregulation of Muc2 and ZO-1 in mouse colonic organoids.DiscussionThese findings demonstrate that MGQD alleviates intestinal barrier dysfunction caused by V. parvula, providing novel mechanistic insight for the management of chronic colitis.

ETHNOPHARMACOLOGICAL RELEVANCE:Myelodysplastic syndromes (MDS) are haematological malignancies for which traditional Chinese medicine (TCM) has been shown to provide distinctive clinical value. Qinghuang powder (QHP), a traditional Chinese medicinal preparation, has been shown to possess significant therapeutic potential in the treatment of myelodysplastic syndrome (MDS). The composition of QHP includes Indigo naturalis, which is known to produce indirubin, and Realgar, a substance that contains As2S2.Notably, QHP has been observed to alleviate MDS symptoms and delay disease progression.However, the precise pharmacological mechanisms by which QHP exerts its effects, particularly with regard to the protection and remodeling of the senescent and metabolically impaired bone marrow stromal niche (e.g., bone marrow mesenchymal stem cells, BMMSCs), remain to be fully elucidated. AIM OF THE STUDY:The present study uniquely shifts the therapeutic focus from hematopoietic malignant clones to the stromal microenvironment, with the aim of exploring the potential mechanisms by which QHP's core components (As2S2 and indirubin) mitigate MDS-associated BMMSC senescence and ameliorate metabolic imbalance. MATERIALS AND METHODS:An in vitro co-culture system was established, comprising patient-derived BMMSCs and the MDS cell line SKM-1. The system was treated with As2S2 and indirubin, the core active components of Qinghuang powder (QHP). Subsequent evaluations of cellular senescence, SASP, and metabolic profiles were systematically conducted using SA-β-Gal staining, Seahorse metabolic assays, ELISA, flow cytometry, qPCR, and Western blotting. RESULTS:In comparison with healthy controls, MDS-BMMSCs demonstrated impaired proliferation, significantly elevated SA-β-Gal positivity (P < 0.001), and increased expression of senescence-associated proteins, including p16, p21, and p53 (P < 0.05). This resulted in a senescence phenotype, characterised by cell cycle arrest without significant pro-inflammatory secretion (P > 0.05). It is noteworthy that co-culture with SKM-1 cells significantly exacerbated this senescent state, resulting in substantial secretion of pro-inflammatory SASP factors (e.g., IL-6, P < 0.05; IL-8, P < 0.001) and the triggering of severe metabolic dysregulation, characterised by NAD+ depletion (P < 0.0001), mitochondrial impairment, and abnormal glycolytic compensation. Following QHP intervention, SA-β-Gal positivity (P < 0.001) and the secretion of pro-inflammatory cytokines (IL-6, P < 0.05; IL-8, P < 0.001) were significantly downregulated. In addition, QHP exhibited a partial amelioration of the cellular energy status, as evidenced by a significantly increased NAD+/NADH ratio (P < 0.001) and the upregulation of SIRT1 expression (P < 0.05). Concurrently, QHP effectively suppressed the abnormally elevated glycolytic reserve capacity (P < 0.05), leading to decreased absolute ATP levels and an elevated ADP/ATP ratio (P < 0.05). Mechanistic analyses indicated that the QHP-induced downregulation of the key senescence protein p16 (P < 0.01) is closely associated with the activation of the energy sensor AMPK (P < 0.05) and the modulation of the epigenetic regulator EZH2, characterised by a significant upregulation of EZH2 mRNA (P < 0.01) alongside a concurrent downregulation of EZH2 protein (P < 0.05). CONCLUSION:This study proposes a novel microenvironment-targeted paradigm for QHP. The presence of MDS tumour cells has been demonstrated to induce a significant state of senescence and metabolic fragility in BMMSCs, accompanied by inflammatory secretion. The active components of QHP have been demonstrated to alleviate BMMSC senescence and partially ameliorate metabolic abnormalities. These microenvironmental remodeling effects may involve the selective curtailment of abnormal glycolysis and may be involved in or associated with the regulation of the AMPK/EZH2 signalling axis.,highlighting the immense potential of targeting stromal metabolic vulnerabilities with TCM in haematological malignancies.

Collagenous gastritis (CG) is a rare chronic inflammatory disorder defined histologically by a subepithelial collagen band exceeding 10 μm, together with a chronic inflammatory infiltrate within the lamina propria. First described in 1989, CG presents with a striking age-stratified dichotomy. The pediatric phenotype is dominated by treatment-refractory iron-deficiency anemia and chronic abdominal pain, with disease usually confined to the stomach. The adult phenotype is dominated by chronic watery diarrhea and frequently coexists with collagenous colitis as part of a broader collagenous gastroenteropathy spectrum. The pathogenesis is widely held to be immune-mediated. Strong associations exist with autoimmune conditions, including celiac disease, common variable immunodeficiency (CVID), and systemic lupus erythematosus (SLE). Recent gene-expression and single-cell studies have identified mixed T-helper 1 (Th1) and T-helper 2 (Th2) cytokine profiles in gastric tissue, together with α4β7-mediated mucosal homing of activated CD4+ T cells, suggesting complex immune dysregulation rather than a primary disorder of collagen biosynthesis. Implicated triggers include certain medications—notably olmesartan—and, more speculatively, infectious agents; a single case report has increased the possibility of Epstein–Barr virus (EBV) reactivation. A single proteomics study has identified reduced epidermal growth factor (EGF) expression as a candidate biomarker, suggesting impaired mucosal repair, although further validation is needed. Diagnosis demands a high index of clinical suspicion and rests on histopathological examination of multi-site gastric biopsies since endoscopic appearances range from normal mucosa to characteristic nodular patterns. Management is empirical and individualized: symptomatic support with proton pump inhibitors (PPIs) and iron supplementation, anti-inflammatory therapy with topically targeted budesonide, dietary intervention in selected patients, and emerging mechanism-targeted approaches including α4β7 blockade. This narrative review synthesizes 101 articles published between 1989 and 31 August 2025, describing approximately 730 histopathologically confirmed CG cases (≈40% pediatric, ≈60% adult; overall female-to-male ratio ≈2.1:1). Replicated findings are distinguished throughout from those based on single reports, with preliminary observations explicitly flagged as hypothesis-generating.

Objectives:To anticipate future trends in science and technology related to traditional Chinese medicine(TCM)and guide cutting-edge research directions,the China Association of Chinese Medicine(CACM)organized experts to deliberate and propose pivotal scientific questions,engineering challenges,and industrial technology issues in the TCM field for 2025.The aim is to address core bottlenecks impeding the high-quality development of TCM through original scientific research,thereby providing strategic technological support for improving the consistency of clinical efficacy,ensuring the sustainable utilization of resources,advancing intelligent industrial upgrading,and enhancing international influence. Methods:In accordance with the targeted commission requirements of the China Association for Science and Technology(CAST)and considering the disciplinary distribution characteristics,the CACM established an expert panel comprising five strategic scientists.Drawing on the major scientific questions selected by CAST and the CACM in previous years,the panel carried out a systematic process of deliberation and discussion,collation and review,evaluation and screening,as well as validation and refinement.Ultimately,two frontier scientific questions,one engineering challenge,and two industrial technology issues were identified and submitted to CAST. Results:This report focuses on key bottlenecks in transforming TCM from empirical inheritance to precision-driven science.It systematically elaborates on five core issues:the two frontier scientific questions aim to uncover the modern scientific underpinnings of classical TCM theories(e.g.,the spleen deficiency theory)and the core efficacy of Daodi Herbs;the engineering challenge is dedicated to constructing intelligent reasoning AI models capable of clarifying the scientific principles underlying TCM-based prevention and treatment of complex diseases(e.g.,gastric cancer);the two industrial technology issues address pressing industrial demands,namely,key technologies for the stable production of"three-excellence"medicinal materials based on molecular pharmacognosy,and the establishment of a quality homogenization technology system for TCM solid preparations based on multimodal data fusion. Conclusions:The five major scientific questions and engineering challenges selected and reported herein systematically target the core bottlenecks and frontier directions in TCM modernization,exhibiting distinct strategic,interdisciplinary,and forward-looking attributes.The development of TCM in the new era must be driven by cutting-edge multidisciplinary technologies to thoroughly elucidate the scientific core of traditional wisdom,thereby achieving comprehensive modernization covering basic research,industrial technology,and clinical application.This will lay a solid foundation for gaining strategic advantages in the global competition of traditional medicine science and technology.

Introduction Branch-duct intraductal papillary mucinous neoplasms (BD-IPMNs) are premalignant pancreatic cystic lesions managed by imaging surveillance or surgical resection. No pharmacological therapy has been established to alter their natural history. Case presentation A 64-year-old Chinese man was incidentally found in April 2023 to have a pancreatic tail cystic lesion. In December 2023, concordant findings on magnetic resonance imaging with cholangiopancreatography (MRI/MRCP) and linear-array endoscopic ultrasound (EUS) established a presumptive diagnosis of BD-IPMN: a unilocular cystic lesion (18.2 × 17.2 mm on EUS) with internal septations, smooth walls, and unequivocal communication with the main pancreatic duct, without worrisome features or high-risk stigmata. Beginning September 2023, the patient received individualized Chinese herbal medicine (CHM) decoctions for concurrent chronic gastritis and functional gastrointestinal symptoms. Over 26 months, the formulation evolved into a stabilized 17-herb prescription designated the Qing-Gan-Jian-Pi-Yi-Shen Decoction (QGJPYS). Serial contrast-enhanced MRI documented cyst stability at approximately 15 mm through September 2024, reduction to 7 mm by March 2025, and non-visualization by December 2025. No anti-neoplastic agents or interventional procedures were administered. Discussion This case documents sustained radiographic resolution of a pancreatic cystic lesion with imaging-confirmed ductal communication in temporal association with CHM therapy. We emphasize that radiographic cyst disappearance is not equivalent to histological eradication of the underlying neoplastic epithelium, and that continued imaging surveillance remains clinically indicated because of the recognized field-effect risk of concomitant pancreatic ductal adenocarcinoma. The observation is hypothesis-generating and supports prospective investigation of integrative approaches in the management of low-risk pancreatic cystic neoplasms.

INTRODUCTION:Due to the incessant advancements in burn treatment technology, the cure rate among patients with severe burns has significantly improved. However, acute lung injury/acute respiratory distress syndrome secondary to severe burns remains one of the challenges in the treatment of severe burns. Exosomes play a role in information and material exchange by transporting lipids, miRNA, proteins, mtDNA, and other substances to target cells. This study primarily explores the role and molecular mechanism of exosomal miRNA in peripheral blood after burn injury in acute lung injury. METHOD:From September 2021 to August 2023, data on severely burned patients treated in our hospital were collected. Based on the new global criteria for ARDS, these severely burned patients were divided into the ARDS group and the non-ARDS group. Exosomes from peripheral blood of severely burned patients collected 4-7 days post-injury were extracted using ultracentrifugation; Exosomes were identified using transmission electron microscopy, NTA, and exosome marker proteins CD63 and CD9. The Hsa-miR-335-3p in the two groups of exosomes were analyzed using RT-qPCR. After labeling exosomes with PKH 67 dye and co-culturing them with BEAS-2B cells, the uptake of exosomes by the cells was observed using confocal microscopy. The dual-luciferase gene reporter assay verified the specific binding of Hsa-miR-335-3p to the 3'-UTR region of TLR4 mRNA. The expression levels of proteins such as TLR4, Bcl-2, BAX, and C-caspase 3 were detected using Western blot. After Annexin V/PI double staining, flow cytometry was used to measure the apoptosis rate of cells in each group. TNF-α, IL-1β, and IL-6 in the cell supernatant were determined by ELISA. RESULT:A positive correlation between TBSA, III°, and BI and Hsa-miR-335-3p. A strong correlation between inhalation injury and mechanical ventilation and Hsa-miR-335-3p. Furthermore, a negative correlation between PaO2/FiO2 and Hsa-miR-335-3p. Among ARDS patients undergoing mechanical ventilation, PaO2/FiO2 still showed a negative correlation with Hsa-miR-335-3p. The results of ROC curve analysis showed that Hsa-miR-335-3p had high sensitivity and specificity (0.944 and 0.819) for the diagnosis of post-burn ARDS, with an area under the curve of 0.907. Exosomes could be uptake by BEAS-2B cells. Exosomes delivered Hsa-miR-335-3p, which inhibited the expression of TLR4 protein in BEAS-2B cells. The results of the dual-luciferase gene reporter assay suggest that Hsa-miR-335-3p specifically binds to the 3'-UTR region of TLR4 mRNA, promoting the degradation of TLR4 mRNA and inhibiting its expression. In the burn microenvironment, Hsa-miR-335-3p protects against BEAS-2B cells apoptosis and mitigates inflammatory responses. Modulating TLR4 affects Hsa-miR-335-3p in protecting against cell apoptosis and reducing inflammatory responses. Hsa-miR-335-3p protects against burn lung injury by through the PI3K/AKT/NF-κB pathway. CONCLUSION:Hsa-miR-335-3p in peripheral blood exosomes from severely burned patients is positively correlated with the severity of burns and negatively correlated with PaO2/FiO2. It exhibits high sensitivity and specificity in the diagnosis of ARDS. Exosomes deliver Hsa-miR-335-3p to lung epithelial cells, negatively regulating the expression of TLR4. Through the PI3K/AKT/NF-κB pathway, it inhibits apoptosis and reduces inflammatory responses, thereby mitigating lung epithelial cell damage caused by severe burns.

ObjectivesThe causal relationship between gut microbiota and lactose intolerance (LI) remains elusive due to confounding factors in observational studies. This study aims to decipher the bidirectional causal link between specific gut bacterial taxa and LI by integrating genetic inference with experimental validation.MethodsWe employed a two-sample bidirectional Mendelian Randomization (MR) analysis using summary statistics from the MiBioGen Consortium (gut microbiota) and the FinnGen study (LI). Robustness was assessed via inverse-variance weighted (IVW), MR-Egger, and sensitivity analyses. To validate the genomic findings, we established a lactose-intolerant rat model induced by a high-lactose diet and analyzed cecal microbiota composition using 16S rRNA high-throughput sequencing.ResultsMR analysis identified significant causal associations: the class Deltaproteobacteria, genus Bilophila were identified as potential risk factors for LI, whereas the genus Paraprevotella and Blautia exhibited protective effects. Notably, reverse MR analysis suggested that LI genetically influences host gut microbiota, particularly suppressing carbohydrate metabolism and blooming Bifidobacterium. Experimental sequencing in rats corroborated these findings, showing a distinctive alteration in microbial structure, specifically an increased abundance of Bifidobacterium and a depletion of Blautia in the high-lactose group, consistent with the genetic inference.ConclusionThis study provides robust evidence for a causal interplay between gut microbiota and LI. The convergence of genetic and experimental data highlights specific taxa, particularly Bifidobacterium and Blautia, as potential biomarkers or therapeutic targets. These findings offer new insights into the microbial etiology of metabolic disorders and suggest microbiota-targeted strategies for LI management.

Stearoyl‑CoA desaturase‑1 (SCD1) has emerged as a critical nexus linking lipid metabolic reprogramming to the regulation of cell death. Frequently overexpressed in digestive system malignancies ‑ including gastric, liver and colorectal cancers ‑ SCD1 represents a promising therapeutic target. This review systematically examined how SCD1, through its lipid‑modifying functions, governs three key forms of regulated cell death ‑ ferroptosis, autophagy and apoptosis ‑ thereby driving malignant progression and mediating therapy resistance in digestive cancers. Building on this mechanistic framework, the specific contributions of these regulatory pathways to tumor biology and their association with drug resistance were delineated. Current preclinical therapeutic strategies targeting SCD1 were then highlighted, encompassing both monotherapy and combination approaches with ferroptosis inducers, chemotherapeutic agents or targeted drugs. Finally, key challenges and outline future directions for drug development and clinical translation in this rapidly evolving field were discussed.

Gastric cancer remains a leading cause of cancer mortality. The Correa cascade-stepwise progression from inflammation through atrophic gastritis, metaplasia and dysplasia to adenocarcinoma-has long defined its pathogenesis. Lineage tracing, single-cell multi-omics and organoid models now reveal marked cellular heterogeneity, plasticity and non-sequential trajectories. This review synthesises gastric stem-cell identity, niche architecture and precancerous progression. Homeostasis is sustained by cycling antral LGR5+ basal and IQGAP3+ isthmus progenitors and by quiescent corpus MIST1+/TROY+ chief-cell reserves, coordinated by Wnt/R-spondin, Notch, BMP, Hedgehog and EGFR signalling. Helicobacter pylori subverts this niche through type-IV-secretion-system delivery of cytotoxin-associated gene A and through BMP collapse, driving region-specific trajectories. In the antrum, hyperproliferation and CDX2-dependent intestinal metaplasia advance to TP53/KRAS/APC-mutant dysplasia. In the corpus, oxyntic atrophy triggers isthmus expansion via type-2 innate lymphoid cell (ILC2)-derived WNT5A and YAP signalling, alongside a tuft-cell-ILC2 interleukin-25/interleukin-13 circuit driving spasmolytic polypeptide-expressing metaplasia (SPEM). In lineage-tracing models, KrasG12D-mutant isthmus cells can also bypass SPEM to generate dysplasia directly. Further origins include ATOH1-deficient pit cells and bone-marrow-derived epithelial hybrids. Together, these findings support a regionally stratified, stem-cell-centred model in which metaplasia and dysplasia arise as parallel cellular fates. This refinement operates at the cellular level without displacing the tissue-level Correa sequence documented in long-term human cohorts. It nominates the remodelled stem-cell niche as a tractable pharmacological target and warrants molecular profiling of at-risk progenitor populations to complement, rather than replace, histopathological surveillance.

The efficacy of Gegen-Qinlian Decoction (GQD) and its modified formula (MGQD) against ulcerative colitis (UC) with damp-heat syndrome (UC-DHS) is closely linked to gut microbiota-mediated biotransformation. Using UHPLC-QTOF-MS/MS, this study profiled GQD and MGQD in artificial gastrointestinal fluids (AGF) and after incubation with gut microbiota from healthy individuals (HI) and UC patients with spleen deficiency syndrome (UC-SDS) and UC patients with UC-DHS. A custom-built MS data analysis workflow was developed to characterize the metabolic profiles of GQD and MGQD. The profiles comprised metabolized prototype constituents, metabolites, pathways, and metabolic rates. The results showed that GQD/MGQD remained stable in AGF. The HI, UC-SDS, and UC-DHS gut microbiota metabolized 52/60, 39/43, and 35/35 GQD/MGQD prototype compounds, resulting in 25 (GQD) and 28 (MGQD) metabolites common to all groups. All three groups exhibited similar metabolic pathways, predominantly deglycosylation to produce aglycones. However, the HI group demonstrated the highest metabolic capability, followed by UC-SDS and then UC-DHS, with superior metabolic rates, lower residual compounds, and higher metabolite abundance. Notably, the addition of two herbs to MGQD did not alter the core metabolic pathways of GQD-sourced constituents but inhibited the biotransformation of certain constituents. Further analysis revealed that glycoside metabolic rates depended on structural features: flavonoid glycosides were metabolized fastest, followed by phenylethanoid glycosides and saponins; among sugar moieties, glucosides were fastest, followed by glucuronides, xylosides, arabinosides, and apiosides. This study reveals the metabolic profiles of GQD/MGQD across different gut microbiota groups (HI, UC-SDS, UC-DHS) and provides a practical analytical workflow for herb-microbiota interaction research.

Background and aimCurrently, the preparation and evaluation of botanical placebos for decoctions lack standardization. This study conducted a multidimensional evaluation of an inert excipient decoction placebo for Chaihu-Shugan-San (CSS) and three low-dose CSS formulations, to determine the optimal CSS formulation for use in the control group of clinical randomized controlled trials. The Four Pillars of Best Practice in Ethnopharmacology guided the analysis.Materials and MethodsCSS was diluted 40-fold, 20-fold, and 10-fold, according to traditional simulated decoction production methods, to obtain 2.5% CSS, 5% CSS, and 10% CSS formulations. These were evaluated together with a pure excipient placebo (pure excipient PBO), consisting solely of excipients and additives. Four CSS decoction formulations were compared for color, odor, and taste using a human scoring method (Likert scale, n = 30). Along with intelligent sensory tools such as a colorimeter, electronic nose, and electronic tongue. Concurrently, the potential pharmacological effects of 4 CSS decoction formulations were examined in animal experiments, including gastric emptying and small intestinal propulsion (n = 80), hot plate analgesia, and the xylene ear swelling test (n = 49).ResultsManual scoring method indicated that the 10% CSS, 5% CSS and 2.5% CSS (difference, 1.57, 1.26 and 0.96 points, respectively, P < 0.01, power = 0.95) scored higher than the pure excipient PBO, with no significant difference in similarity between 5% CSS and 10% CSS (P > 0.05, power = 0.95). The intelligent sensory instrument results revealed that pure excipient PBO displayed the closest color match to the CSS decoction (ΔE = 2.05), while 10% CSS most closely approximated the CSS decoction in odor. Taste differences between the 4 CSS formulations and CSS were significant. Pharmacological studies found no statistically significant differences between the 4 CSS formulation groups and the control group in gastric emptying rate or small intestine propulsive motility (P > 0.05, power = 0.95) nor in ear swelling intensity (H = 8.935, P = 0.177) or pain threshold (P > 0.05, power = 0.004).Conclusion10% CSS and 5% CSS, while most similar in appearance to the CSS decoction, did not show superior in improving gastrointestinal motility, anti-inflammatory properties, or analgesic efficacy. However, their safety profile still requires future validation through animal models and quantitative mass spectrometry analysis.

OBJECTIVE:To explore whether Gegen Qinlian decoction (, GQD) targets ferroptosis pathway to ameliorate experimental colitis in mice. METHODS:A mice model of dextran sulfate sodium (DSS) induced colitis was established and therapeutic effects of GQD were determined by detecting body weight, disease activity index (DAI), colon length and histopathological changes. Then, the expression levels of inflammatory cytokines were detected by enzyme-linked immunosorbent assay, the expression levels of tight junction proteins were detected by immunohistochemistry and the expression levels of ferroptosis-associated proteins were detected by western blotting. RESULTS:GQD treatment attenuated weight loss and DAI score, increased colon length, ameliorated intestinal histopathological damage, inhibited colonic inflammatory cytokine release and enhanced epithelial barrier function in mice with ulcerative colitis (UC). Furthermore, GQD administration obviously improved the expression of ferroptosis-associated proteins (solute carrier family 7 member 11 and acyl-CoA synthetase long chain family member 4). CONCLUSION:GQD could exert a therapeutic effect on colitis by alleviating colon damage and promoting intestinal mucosal barrier repair in DSS-induced colitis mice through the inhibition of ferroptosis, which may provide an effective natural therapy for the treatment of UC.