BACKGROUND:Ulcerative colitis (UC) is a chronic, non-specific inflammatory bowel disease. The gut microbiome undergoes significant changes in UC. Fatigue is a highly prevalent and debilitating extraintestinal symptom of UC, which negatively affects quality of life. However, its relationship with gut microbes and metabolites remains unclear. AIM:To assess the gut microbiota and metabolomic characteristics of patients with UC with fatigue (HUCF). METHODS:A total of 120 participants were recruited and divided into four groups (n = 30 per group) based on the diagnosis of UC and Fatigue Scale-14 scores: HUCF, UC without fatigue (HUCN), healthy with fatigue (HHF), and healthy without fatigue (HHN). Fresh stool samples were collected for 16S rRNA sequencing and untargeted metabolomic analysis. RESULTS:Metabolomic analysis revealed significant differences among the four groups (principal component analysis/partial least squares discriminant analysis, P = 0.001), with differential expression of metabolites such as linoleoyl ethanolamide, arachidonoyl ethanolamide, glycocholic acid, and thromboxane (TX). Notably, TX was detected only in the HUCF group. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis revealed alterations in eicosanoid, tryptophan, and tyrosine metabolism in the HUCF group. Microbial richness and diversity were significantly lower in the HUCF group than in the other three groups. The HUCF group showed enrichment of Hyphomicrobiales, Brucella, Eisenbergiella, Pediococcus, and Sellimonas. The HUCN group showed enrichment of Campylobacter-related taxa. The HHF group showed enrichment of Fusobacterium, Desulfovibrionaceae, and Bilophila. The HHN group showed enrichment of beneficial genera such as Adlercreutzia. Notably, Anaerococcus, a beneficial genus, was enriched in the HUCF group. Correlation analysis indicated that specific microbes (e.g., Faecalibacterium and Escherichia-Shigella) were associated with the severity of UC and fatigue. CONCLUSION:Patients with HUCF exhibit a distinct gut microbial structure and metabolomic profile. The pro-inflammatory metabolite TX and the genus Anaerococcus are uniquely enriched in patients with HUCF, suggesting their potential roles in the development of HUCF. These findings provide novel insights and a theoretical basis for improving the clinical management of HUCF.

Background: CHB patients with NAs still suffer from TCM symptoms which affect the quality of life varying severity. The pathogenesis of CHB in TCM is the accumulation of damp-heat, while there are sub-types of damp heat syndrome. Objective: To evaluate the clinical efficacy and safety of Yinchen Wuling powder combined with NAs on CHB patients of damp-heat and damp-predominant syndrome, while investigate the potential mechanisms and novel applications of classical prescriptions through network pharmacology combined with metabolomics. Design setting participants and intervention: It was a randomized, placebo-controlled clinical study at 3 hospitals in Shanghai. A total of 62 participants diagnosed with damp-heat and damp-predominant syndrome of CHB patients with NAs were randomly allocated to receive either Yinchen Wuling powder or placebo; the therapy consisted of 8.4 g dosage, administered twice a day after meals for a duration of 4 weeks. Blood samples were collected for non-targeted metabolomics research of characteristic metabolites of CHB patients and pathways enriched by YCWLP treatment. The metabolic network and target of YCWLP on CHB patients of damp-heat and damp-predominant syndrome was constructed by the integration of network pharmacology and non-targeted metabolomics.

Yinchenhao decoction (YCHD) is widely used in the treatment of damp-heat syndrome of chronic hepatitis B (CHB), but it remains unclear about the active compounds in YCHD and its potential mechanism for treating CHB. The purpose of this work is to evaluate the clinical efficacy of YCHD combined with nucleoside analogues (NAs) for the treatment of CHB. Besides, based on the exact clinical efficacy, we combined serum metabolomics and network pharmacology to screen differential metabolites and related pathways regulated by YCHD to investigate the possible mechanism for treating CHB. It revealed that NAs plus YCHD could significantly improve alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, increase HBV-DNA negative rate (P<0.05), reduce the levels of inflammatory factors and LSM (both P<0.05), regulate lipids (P<0.05), and improve the symptoms of traditional Chinese medicine (TCM) (P<0.05) in CHB patients. YCHD was relatively safe. It showed 30 active compounds including chlorogenic acid, geniposide, emodin, quercetin, kaempferol, β-sitosterol and aloe emodin, and 115 key targets which were related to the regulation of lipids and reduction of oxidative stress related to the effect of YCHD in CHB in the network pharmacology analysis. We found 9 core targets and 4 key metabolites according to metabolomics, which were partly consistent with the network pharmacology findings. It proved that network pharmacology combined with metabolomics can well explain the "multi-component-multi-target" mechanism of complex TCM.

Background Ulcerative colitis (UC) is a chronic non-specific inflammatory intestinal disease, categoried under "dysentery" and "intestinal bleeding" in Traditional Chinese Medicine (TCM). Jianpi Qingchang decoction (JPQC) is a combination formula specifically designed for the treatment of UC. The primary objective of this study is to examine the clinical efficacy of JPQC in individuals diagnosed with UC who exhibit both spleen deficiency and dampness-heat syndrome, along with the presence of fatigue. The investigation will focus on assessing the impact of JPQC on the gut microbiota and metabolites in these patients, aiming to elucidate the regulatory mechanism that JPQC exerts on the gut microbiota and metabolites in the context of UC-related fatigue. Methods In this randomized clinical trial, 140 subjects diagnosed with UC will be recruited and randomized into two groups. They will receive either JPQC combined with mesalazine or mesalazine alone for 12 weeks. Follow-up visits will be conducted every four weeks, with a post-treatment visit scheduled at 6 months. The primary outcome measures include the Inflammatory bowel disease fatigue scale(IBD-F). Secondary efficacy indicators comprise the assessment of TCM syndrome and individual syndrome efficacy before and after treatment, Modified Mayo score, Simple clinical colitis activity index (SCCAI), as well as the Inflammatory Bowel Disease Questionnaire (IBDQ) for each group. The other outcomes are the Intestinal microbial diversity and non-targeted metabonomics, which will be measured at baseline and 12 weeks after randomization. Discussion If effective, JPQC will provide substantial clinical evidence concerning the effectiveness and safety in the treatment of patients with UC experiencing spleen deficiency and dampness-heat syndrome accompanied by fatigue. Trial registration ChiCTR2300068348

Portulaca oleracea L. (POL) has a long history of medicinal use worldwide, and numerous clinical and experimental studies demonstrated the therapeutic effects of POL and its active ingredients in the treatment of Ulcerative colitis (UC). In this review, we summarized the underlying mechanisms and roles of POL in UC treatment based on experimental and clinical studies. The research articles cited in this study were obtained by employing specific keywords, such as "purslane", "IBD", "UC", "inflammation", "gut microbiota", and "intestinal barrier", in PubMed, Web of Science, Google Scholar, and China National Knowledge Infrastructure databases. Clinical studies found that both POL monotherapy and POL traditional Chinese medicine compound are effective in treating UC. Meanwhile, experimental studies found that POL intervenes in UC by regulating intestinal flora, repairing mucosal barrier, and regulating immune response. Increasing evidence suggests the therapeutic potential of POL in UC treatment.

Background and AimsMounting evidence highlights a strong association between chronic pancreatitis (CP) and type 2 diabetes (T2D), although the exact mechanism of interaction remains unclear. This study aimed to investigate the crosstalk genes and pathogenesis between CP and T2D.MethodsTranscriptomic gene expression profiles of CP and T2D were extracted from Gene Expression Omnibus, respectively, and the common differentially expressed genes (DEGs) were subsequently identified. Further analysis, such as Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), protein-protein interaction, transcription factors (TFs), microRNA (miRNAs), and candidate chemicals identification, was performed to explore the possible common signatures between the two diseases.ResultsIn total, we acquired 281 common DEGs by interacting CP and T2D datasets, and identified 10 hub genes using CytoHubba. GO and KEGG analyses revealed that endoplasmic reticulum stress and mitochondrial dysfunction were closely related to these common DEGs. Among the shared genes, EEF2, DLD, RAB5A, and SLC30A9 showed promising diagnostic value for both diseases based on receiver operating characteristic curve and precision-recall curves. Additionally, we identified 16 key TFs and 16 miRNAs that were strongly correlated with the hub genes, which may serve as new molecular targets for CP and T2D. Finally, candidate chemicals that might become potential drugs for treating CP and T2D were screened out.ConclusionThis study provides evidence that there are shared genes and pathological signatures between CP and T2D. The genes EEF2, DLD, RAB5A, and SLC30A9 have been identified as having the highest diagnostic efficiency and could be served as biomarkers for these diseases, providing new insights into precise diagnosis and treatment for CP and T2D.

Abdominal pain is a major symptom of inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis, and has a significant impact on patients’ quality of life. Given the evolving understanding of IBD pathology and management strategies, there is an urgent need to review the recent research findings. In this review, we have analyzed the epidemiology, pathophysiology, and management of abdominal pain in IBD over the past decade. We draw on the current literature and highlight emerging trends, challenges, and advances in this field. By synthesizing key findings, this review provides insights into the complex interplay between abdominal pain, disease progression, and therapeutic interventions for IBD.

BACKGROUND Both N6-methyladenosine (m6A) methylation and autophagy are considered relevant to the pathogenesis of ulcerative colitis (UC). However, a systematic exploration of the role of the com-bination of m6A methylation and autophagy in UC remains to be performed. AIM To elucidate the autophagy-related genes of m6A with a diagnostic value for UC. METHODS The correlation between m6A-related genes and autophagy-related genes (ARGs) was analyzed. Finally, gene set enrichment analysis (GSEA) was performed on the characteristic genes. Additionally, the expression levels of four characteristic genes were verified in dextran sulfate sodium (DSS)-induced colitis in mice. RESULTS GSEA indicated that BAG3, P4HB and TP53INP2 were involved in the inflammatory response and TNF-α signalling via nuclear factor kappa-B. Furthermore, polymerase chain reaction results showed significantly higher mRNA levels of BAG3 and P4HB and lower mRNA levels of FMR1 and TP53INP2 in the DSS group compared to the control group. CONCLUSION This study identified four m6A-ARGs that predict the occurrence of UC, thus providing a scientific reference for further studies on the pathogenesis of UC.

BACKGROUND Colorectal cancer (CRC) is the third most common cancer worldwide, with the fourth highest mortality among all cancers. Reportedly, in addition to adenomas, serrated polyps, which account for 15%-30% of CRCs, can also develop into CRCs through the serrated pathway. Sessile serrated adenomas/polyps (SSAs/Ps), a type of serrated polyps, are easily misdiagnosed during endoscopy. AIM To observe the difference in the Wnt signaling pathway expression in SSAs/Ps patients with different syndrome types. METHODS From January 2021 to December 2021, patients with SSAs/Ps were recruited from the Endoscopy Room of Shanghai Traditional Chinese Medicine-Integrated Hospital, affiliated with Shanghai University of Traditional Chinese Medicine. Thirty cases each of large intestine damp-heat (Da-Chang-Shi-Re, DCSR) syndrome and spleen-stomach weakness (Pi-Wei-Xu-Ruo) syndrome were reported. Baseline comparison of the general data, typical tongue coating, colonoscopy findings, and hematoxylin and eosin findings was performed in each group. The expression of the Wnt pathway-related proteins, namely β-catenin, adenomatous polyposis coli, and mutated in colorectal cancer, were analyzed using immunohistochemistry. RESULTS Significant differences were observed with respect to the SSAs/Ps size between the two groups of patients with different syndrome types (P = 0.001). The other aspects did not differ between the two groups. The Wnt signaling pathway was activated in patients with SSAs/Ps belonging to both groups, which was manifested as β-catenin protein translocation into the nucleus. However, SSAs/Ps patients with DCSR syndrome had more nucleation, higher β-catenin expression, and negative regulatory factor (adenomatous polyposis coli and mutated in colorectal cancer) expression (P < 0.0001) than SSA/P patients with Pi-Wei-Xu-Ruo syndrome. In addition, the SSA/P size was linearly correlated with the related protein expression. CONCLUSION Patients with DCSR syndrome had a more obvious Wnt signaling pathway activation and a higher risk of carcinogenesis. A high-quality colonoscopic diagnosis was essential. The thorough assessment of clinical diseases can be improved by combining the diseases of Western medicine with the syndromes of traditional Chinese medicine.

溃疡性结肠炎在临床治疗中存在反复发作、迁延不愈的困惑,中西医结合的诊疗方案有助于促进患者黏膜愈合,临床缓解,从而提高患者生存质量.文章总结了唐志鹏教授治疗UC的临证经验,唐志鹏教授认为UC是本虚标实之症,在健脾益气,清利湿热,活血化瘀的基础上提出"半以痢治,半以痈治"论治UC屡获良效.附医案一则为佐证.

OBJECTIVE:To explore the therapeutic effect and mechanism of Dachengqi decoction on patients with mild acute pancreatitis (MAP).METHODS:A parallel randomized controlled trial was conducted. Sixty-eight patients with acute pancreatitis (AP) admitted to Shanghai Traditional Chinese Medicine (TCM)-Integrated Hospital from March 2018 to February 2021 were enrolled. Referring to the condition on admission of the patients and whether they agreed to receive the Dachengqi decoction or not, they were divided into conventional treatment group and Dachengqi decoction group according to the principle of 1:1 equal randomness. Meanwhile, 20 healthy volunteers were recruited as controls. Both groups of patients were treated with octreotide, fasting, gastrointestinal decompression, antipyretic and analgesic, anti-inflammatory, inhibition of gastric acid and pancreatic juice secretion, maintenance of electrolyte balance and other western conventional medicine. The patients in the Dachengqi decoction group received Dachengqi decoction orally on the basis of routine treatment, 100 mL each time, twice a day, for seven consecutive days. The inflammation parameters [white blood cell count (WBC), C-reactive protein (CRP), procalcitonin (PCT), interleukin-6 (IL-6)] before and after treatment and the recovery time of gastrointestinal function (first exhaust time, time to recover bowel sounds, first defecation time) of patients were recorded. 16S rRNA gene sequencing of stool samples was recorded, and normalized data were obtained after quality control and other related processing. The data were subjected to diversity analysis (Alpha diversity and Beta diversity) and linear discriminant analysis effect size analysis (LEfSe analysis) to observe changes in the gut microbiota of MAP patients. Spearman rank correlation coefficient was used to analyze the correlation between inflammatory indexes and microorganisms at the intestinal genus level. Blood, urine, stool samples, renal function, and electrocardiogram (ECG) during treatment of MAP patients were detected to assess the safety of the treatment.RESULTS:Of the 68 patients with AP, 16 were excluded from moderate-severe AP, 4 were not collected or voluntarily abandoned treatment. Finally, 48 patients with MAP were enrolled, 24 in the conventional treatment group and 24 in the Dachengqi decoction group. The inflammation parameters levels at 7 days of treatment in both groups were significantly lower than those before treatment. CRP, PCT and IL-6 levels in the Dachengqi decoction group were significantly lower than those in the conventional treatment group [CRP (mg/L): 8.50 (3.50, 13.00) vs. 16.00 (9.25, 29.75), PCT (μg/L): 0.06 (0.03, 0.08) vs. 0.09 (0.05, 0.11), IL-6 (ng/L): 6.36 (3.96, 10.79) vs. 13.24 (6.69, 18.87), all P < 0.05]. The first exhaust time, time to recover bowel sounds and first defecation time in the Dachengqi decoction group were significantly shorter than those in the conventional treatment group [first exhaust time (days): 1.62±0.65 vs. 2.80±0.65, time to recover bowel sounds (days): 1.13±0.58 vs. 2.31±0.76, first defecation time (days): 3.12±0.75 vs. 4.39±0.76, all P < 0.05]. The analysis of intestinal microflora diversity showed that both the diversity and abundance of microbial communities were the highest in the healthy control group and the lowest in the conventional treatment group. In addition, the coincidence degree of microbial communities in healthy controls and MAP patients was small, while the coincidence degree of MAP patients among different treatment methods was relatively large. LEfSe analysis showed that Dachengqi decoction reduced the relative abundance of Escherichia coli-Shigella and Clostridium erysipelae, and increased the relative abundance of three beneficial bacteria, namely Lactobacillus, Rombutzia and Brutella. In the intestines of MAP patients, Lactobacillus mucilaginus and Lactobacillus conjunctus were significantly enriched. Correlation analysis showed that positive correlations between Escherichia coli-Shigella and the four inflammatory indicators including WBC, CRP, PCT, IL-6 were statistically significant (r value was 0.31, 0.41, 0.57, 0.43, respectively, all P < 0.05). There was no significant correlation between other bacteria and inflammatory indicators. During the treatment, there was no obvious abnormality in blood, urine and feces, renal function and ECG of MAP patients.CONCLUSIONS:Dachengqi decoction could reduce inflammatory responses and promote recovery of intestinal microecological balance and gastrointestinal function in patients with MAP by regulating the composition of intestinal flora. No significant adverse effects were observed during the treatment period.

Background: The recurrence of colorectal adenomas (CRAs) after endoscopy predisposes patients to a risk of colorectal cancer. Guided by the traditional Chinese medicine (TCM), patients with colorectal diseases usually manifest with spleen deficiency syndrome (SDS) and are treated with Sijunzi decoction (SJZD). Therefore, this trial aims to explore the efficacy and safety of SJZD in the prevention and treatment of CRAs recurrence.Methods: SJZD on prevention and treatment of CRAs recurrence after resection: a multicenter, randomized, double-blind, placebo-controlled trial was designed. Patients who undergo polypectomy of CRAs will be recruited and randomized into a SJZD group and a placebo group in a 1:1 ratio. The intervention phase will be 12 months. The follow-up period will last 24 months. The primary outcome is the CRA recurrence rate after intervention. The secondary outcomes include the CRA recurrence rate at the second year post-polypectomy, the pathological type of adenoma and the alterations in SDS scores after intervention.Discussion: Previous clinical practice has observed the sound effect of SJZD in the context of gastrointestinal diseases. A number of experiments have also validated the active components in SJZD. This trial aims to provide tangible evidence for the usage of SJZD, hoping to reduce the recurrence of CRAs.

[目的]观察白藜芦醇(Res)对四氯化碳(CCl4)诱导的小鼠肝纤维化(HF)的干预作用及其对肝脏生物钟的调节效应.[方法]本实验采用雄性C57BL/6小鼠,将小鼠按体质量随机分成对照组、模型组、白藜芦醇组,每组10只.模型组及白藜芦醇组按2.5 mL/kg腹腔注射体积分数为20％CCl4油剂溶液进行造模,一周两次,连续4周,对照组按同等剂量同等频次给予腹腔注射橄榄油.白藜芦醇以生理盐水稀释呈终浓度为30 mg/kg进行腹腔注射干预,每日1次,连续4周,对照组及模型组给予等量生理盐水按同等频次腹腔注射.4周后处死小鼠并收集血清及肝组织样本.采用病理组织切片苏木精-伊红(HE)染色、马松(Masson)染色、天狼星红(Sirius Red)染色观察肝纤维化情况,全自动生化分析仪测定小鼠血清丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、乳酸脱氢酶(LDH)活性,免疫组织化学检测肝脏α-平滑肌肌动蛋白(α-SMA)、I型胶原(COL-1)评估肝纤维化程度,实时聚合酶链反应(RT-PCR)、蛋白质印迹法(Western blot)检测肝脏生物钟基因Clock、脑和肌肉芳香烃受体核转运样蛋白1(Bmal1)、周期基因1(Per1)周期基因2(Per2)、隐花色素1(Cry1)、隐花色素2(Cry2)的表达.[结果]模型组与对照组相比,肝功能指标如ALT、AST、LDH等均显著升高;病理切片HE染色提示模型组汇管区纤维组织增生,肝小叶间胆管明显增生,部分分割包绕肝小叶使其结构紊乱,Masson染色及Sirius Red染色提示模型组汇管区胶原沉积显著增多,免疫组化显示α-SMA、COL-1阳性面积显著增多;RT-PCR及Western blot结果显示肝脏生物钟基因Clock、Bmal1、Per1、Per2、Cry1、Cry2的mRNA及蛋白表达均显著下降.白藜芦醇干预后可显著逆转上述指标变化.[结论]白藜芦醇可显著减轻CCl4诱导的小鼠肝纤维化,及机制可能与调控肝脏生物钟基因有关.

BACKGROUND Bone loss and osteoporosis are commonly described as extra-intestinal manifestations of inflammatory bowel disease (IBD). Jianpi Qingchang Bushen decoction (JQBD) is a prescription used in clinical practice. However, further studies are needed to determine whether JQBD regulates the receptor activator of nuclear factor kappa B (NF-κB) (RANK)/receptor activator of NF-κB ligand (RANKL)/ osteoprotegerin (OPG) pathways and could play a role in treating IBD-induced bone loss. AIM To evaluate the therapeutic effect of JQBD in IBD-induced bone loss and explore the underlying mechanisms. METHODS An IBD-induced bone loss model was constructed by feeding 12 6-to-8-wk-old interleukin-10 (IL-10)-knockout mice with piroxicam for 10 d. The mice were randomly divided into model and JQBD groups. We used wild-type mice as a control. The JQBD group was administered the JQBD suspension for 2 wk by gavage, while the control and model groups were given normal saline at the corresponding time points. All mice were killed after the intervention. The effect of JQBD on body weight, disease activity index (DAI), and colon length was analyzed. Histopathological examination, colon ultrastructure observation, and micro-computed tomographic scanning of the lumbar vertebrae were performed. The gene expression of NF-κB, tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and IL-8 in the colon was evaluated by real-time polymerase chain reaction. Colon samples were assessed by Western blot for the expression of RANKL, OPG, RANK, and NF-κB proteins. RESULTS The model group lost body weight, had a shorter colon, and showed a dramatic increase in DAI score, whereas JQBD had protective and therapeutic effects. Treatment with JQBD significantly improved inflammatory cell infiltration and reduced crypt abscess and ulcer formation. Three-dimensional imaging of the vertebral centrum in the model group revealed a lower bone mass, loose trabeculae, and “rod-shaped” changes in the structure compared to the control group and JQBD groups. The bone volume/total volume ratio and bone mineral density were significantly lower in the model group than in the control group. JQBD intervention downregulated the NF-κB, TNF-α, IL-1β, IL-6, and IL-8 mRNA expression levels. The RANKL and OPG protein levels were also improved. CONCLUSION JQBD reduces inflammation of the colonic mucosa and inhibits activation of the RANK/ RANKL/OPG signaling pathway, thereby reducing osteoclast activation and bone resorption and improving bone metabolism.

Background . Excessive endoplasmic reticulum (ER) stress in intestinal epithelial cells (IEC) may lead to impaired intestinal mucosal barrier function and then participate in the pathogenesis of ulcerative colitis (UC). Jianpi Qingchang decoction (JPQCD) has been shown to have protective effects on UC. However, further studies are needed to determine whether JPQCD regulates PERK/eIF2 α /ATF4/CHOP pathways to play a role in treating UC. Methods . IL-10 −/− mice were randomly assigned into five groups: control, model, low-dose JPQCD (JPQCD L), middle-dose JPQCD (JPQCD M), and high-dose JPQCD (JPQCD H). All groups except for the control group were given model feed containing 200 ppm piroxicam for 10 d to induce colitis. As a comparison, we used wild-type mice that were the progeny of IL-10 +/− matings, bred in the same facility. The control group and wild-type mice were fed with common feed. At the same time, mice in each group were given corresponding drugs by gavage for 14 d. The disease activity index of mice in each group was evaluated daily. Colon tissues of mice were collected, colon length was measured, and pathological changes and ultrastructure of colon epithelial cells were observed. The effects of JPQCD on the PERK/eIF2 α /ATF4/CHOP pathways were evaluated by western blotting and reverse transcription-polymerase chain reaction (RT-PCR). The expression of CHOP in colon tissue was detected by tissue immunofluorescence assay. The expression of NF- κ B, p-NF- κ B p65 protein was analyzed by western blotting; the level of IL-17 in colon tissue was detected by enzyme-linked immunosorbent assay (ELISA) and verified by examining NF- κ B and IL-17 mRNA levels by RT-PCR. Results . Compared with the control group, the model group showed significant colitis symptoms and severe colonic tissue damage. The results showed that JPQCD significantly reduced body weight loss, ameliorated disease activity index, and restored colon length in IL-10 −/− mice with piroxicam-induced colitis. Western blotting and RT-PCR showed that the PERK/eIF2 α /ATF4/CHOP pathway was activated in colon tissue of model mice, suggesting that the pathway is involved in the pathogenesis of ulcerative colitis (UC) and could become a potential therapeutic target. The JPQCD treatment inhibited the activation of the PERK/eIF2 α /ATF4/CHOP pathway, alleviated the ER stress, and played a role in preventing and treating UC. In addition, JPQCD can also downregulate the protein of NF- κ B, p-NF- κ B p65, downregulate the mRNA expression of NF- κ B, and reduce the content of IL-17 and its mRNA expression in colon tissues. Conclusion . JPQCD may play a protective role in UC by regulating the PERK/eIF2 α /ATF4/CHOP signaling pathway and relieving endoplasmic reticulum stress.

Decursin possesses the potential to alleviate transforming growth factor (TGF)-beta-induced hepatic stellate cells (HSCs) activation. However, the mechanisms by which decursin alleviates hepatic fibrosis remain not fully understood. Our aim is to explore the function of decursin on regulating HSCs' activation and hepatic fibrosis. The anti-fibrotic effect of decursin was evaluated by Masson and Sirius red staining, and immunohistochemical (IHC) and quantitative real-time PCR (qRT-PCR) analyses for alpha-smooth muscle actin (alpha-SMA) and collagen type I (Col1 alpha 1) expression. Ferroptosis was assessed by measuring iron concentration, glutathione peroxidase 4 (Gpx4), and prostaglandin endoperoxide synthase 2 (Ptgs2) expression, glutathione (GSH) level, lipid peroxidation, and reactive oxygen species (ROS) level. We found that decursin treatment decreased carbon tetrachloride (CCl4)-induced liver fibrosis. The primary HSCs isolated from decursin-treated group showed an increased Fe2+, lipid ROS level, and decreased Gpx4 and GSH levels compared with HSCs from the model group. Moreover, decursin promoted ferroptosis in activated HSCs in vitro, as evidenced by declined Gpx4 and GSH levels, increased Fe2+, ROS, and Ptgs2 levels compared with control. More important, ferroptosis inhibitor destroyed the anti-fibrosis effect of decursin on HSCs. In summary, these data suggest that decursin has potential to treat hepatic fibrosis.

BACKGROUND Ulcerative colitis (UC) is a complicated disease caused by the interaction between genetic and environmental factors that affects mucosal homeostasis and triggers an inappropriate immune response. Single-cell RNA sequencing (scRNA-seq) can be used to rapidly obtain the precise gene expression patterns of thousands of cells in the intestine, analyze the characteristics of cells with the same phenotype, and provide new insights into the growth and development of intestinal organs, the clonal evolution of cells, and immune cell changes. These findings can provide new ideas for the diagnosis and treatment of intestinal diseases. AIM To identify clinical phenotypes and biomarkers that can predict the response of UC patients to specific therapeutic drugs and thus aid the diagnosis and treatment of UC. METHODS Using the Gene Expression Omnibus (GEO) database, we analyzed peripheral blood cell subtypes of patients with UC by scRNA-seq combined with bulk RNA sequencing (RNA-seq) to reveal the core genes of UC. We then combined weighted gene correlation network analysis (WGCNA) and least absolute shrinkage and selection operator (LASSO) analysis to reveal diagnostic markers of UC. RESULTS After processing the scRNA-seq data, we obtained data from approximately 24340 cells and identified 17 cell types. Through intercellular communication analysis, we selected monocyte marker genes as the candidate gene set for the prediction model. Construction of a WGCNA coexpression network identified RhoB, cathepsin D (CTSD) and zyxin (ZYX) as core genes. Immune infiltration analysis showed that these three core genes were strongly correlated with immune cells. Functional enrichment analysis showed that the differentially expressed genes were closely related to immune and inflammatory responses, which are associated with many challenges in the diagnosis and treatment of UC. CONCLUSION Through scRNA-seq analysis, LASSO diagnostic model building and WGCNA, we identified RhoB, CTSD and ZYX as core genes of UC that are closely related to monocyte infiltration that may serve as diagnostic markers and molecular targets for UC therapeutic intervention.

OBJECTIVE:To observe the clinical efficacy of Dachengqi decoction combined with octreotide in the treatment of patients with acute pancreatitis (AP).METHODS:From March 2018 to February 2021, a total of 68 patients with mild acute pancreatitis (MAP) and moderately severe acute pancreatitis (MSAP) admitted to Shanghai Traditional Chinese Medicine-Integrated Hospital were included, and they were randomly divided into western medicine treatment group and Dachengqi decoction group. The patients in the western medicine treatment group received conventional western medicine (octreotide+symptomatic treatment); in the Dachengqi decoction group, 100 mL of Dachengqi decoction was taken orally on the basis of conventional western medicine, twice a day; the observation time for both groups was 7 days. The levels of inflammation parameters [white blood cell count (WBC), interleukin-6 (IL-6), procalcitonin (PCT), C-reactive protein (CRP)] and serum amylase (Amy) before and after treatment of patients between the two groups, as well as the occurrence of clinical efficacy indicators and adverse reactions were compared.RESULTS:Among the 68 included patients, 4 were excluded because the specimen was not obtained or the patient gave up the treatment. A total of 64 patients were finally enrolled in the analysis, including 32 cases in the Dachengqi decoction group and 32 cases in the western medicine treatment group respectively. There was no statistically significant difference in inflammation parameters or serum Amy levels before treatment between the two groups. At 7 days of treatment, the inflammatory parameters and serum Amy levels of the two groups were significantly lower than those before treatment [western medicine treatment group: WBC (×109/L) was 5.94±2.08 vs. 11.81±3.66, IL-6 (ng/L) was 7.22 (5.72, 14.23) vs. 30.13 (15.77, 85.37), PCT (μg/L) was 0.068 (0.052, 0.128) vs. 0.290 (0.231, 0.428), CRP (mg/L) was 26.0 (18.3, 35.8) vs. 112.0 (62.0, 126.0), Amy (U/L) was 77 (57, 116) vs. 352 (162, 1 576); Dachengqi decoction group: WBC (×109/L) was 5.56±2.04 vs. 12.22±2.85, IL-6 (ng/L) was 5.70 (3.26, 11.06) was 50.30 (23.99, 88.32), PCT (μg/L) was 0.038 (0.028, 0.808) vs. 0.308 (0.129, 0.462), CRP (mg/L) was 11.0 (3.5, 24.0) vs. 150.0 (75.0. 193.0), Amy (U/L) was 78 (57, 104) vs. 447 (336, 718); all P < 0.05], and the levels of IL-6, PCT, and CRP decreased more significantly after treatment in the Dachengqi decoction group (all P < 0.05). The total clinical effective rate of patients in the Dachengqi decoction group was significantly higher than that of the western medicine treatment group [93.75% (30/32) vs. 71.88% (23/32), P < 0.05]. There was no obvious adverse event during the treatment and observation period in the two groups.CONCLUSIONS:Dachengqi decoction combined with octreotide therapy could improve the clinical efficacy of AP patients, and its mechanism might be related to reducing the level of inflammatory factors, thereby inhibiting the inflammatory response, and regulating the level of serum Amy.

Scope To investigate the role of endoplasmic reticulum stress (ERS)‐induced autophagy in inflammatory bowel disease (IBD) and the intervention mechanism of Portulaca oleracea L . (POL) extract, a medicinal herb with anti‐inflammatory, antioxidant, immune‐regulating, and antitumor properties, in vitro and in vivo. Methods and Results An IL‐10‐deficient mouse model is used for in vivo experiments; a thapsigargin (Tg)‐stimulated ERS model of human colonic mucosal epithelial cells (HIECs) is used for in vitro experiments. The levels of ERS‐autophagy‐related proteins are examined by immunofluorescence and Western blot. Cellular ultrastructure is assessed with transmission electron microscopy. POL extract promotes a healing effect on colitis by regulating ERS‐autophagy through the protein kinase R‐like endoplasmic reticulum kinase (PERK)‐eukaryotic initiation factor 2α (eIF2α)/Beclin1‐microtubule‐associated protein light chain 3II (LC3II) pathway. Conclusion Overall, the results of this study further confirm the anti‐inflammatory mechanism and protective effect of POL extract and provide a new research avenue for the clinical treatment of IBD.