BACKGROUND:Promoting intestinal barrier repair and epithelial regeneration is a core therapeutic objective in managing ulcerative colitis (UC). Intestinal stem cell (ISC) differentiation is pivotal in sustaining epithelial renewal and mucosal homeostasis. Huangqin decoction (HQD), a classical herbal formulation comprising Scutellaria baicalensis, Ziziphus jujuba, Paeonia lactiflora, and Glycyrrhiza uralensis, is clinically used for inflammatory bowel disease. Nevertheless, how HQD precisely regulates ISC differentiation to promote UC repair remains unclear. PURPOSE:This research sought to assess whether HQD ameliorates UC by concurrently modulating the gut microbiome, tryptophan metabolism, aryl hydrocarbon receptor (AhR) activation, and ISC differentiation. METHODS:Mice developed colitis after drinking water with a 3.5% (w/v) concentration of dextran sulfate sodium. We evaluated HQD effects on colon length, weight trajectory, disease activity index score, histological damage, and colonic inflammatory mediator abundance. Metagenomic sequencing resolved microbiota restructuring, while UPLC-MS/MS quantified fecal tryptophan metabolites such as indole derivatives. AhR pathway activity (AhR, CYP1A1), its downstream cytokine IL-22, and ISC fate were mapped by combining immunofluorescence, ELISA, Western blot, and RT-qPCR, probing Lgr5 for stem-cell identity and MUC2, LYZ, and ChgA for lineage-specific differentiation. The involvement of AhR and gut microbiota was investigated using AhR inhibitors and broad-spectrum antibiotics. RESULTS:High-dose HQD significantly alleviated colitis symptoms, reduced colon damage, and corrected gut dysbiosis. HQD increased the abundance of related bacteria that elevated colonic levels of indole-3-propionic acid, indole-3-acetamide, and tryptamine, acting as AhR ligands that upregulate AhR and its downstream targets CYP1A1 and IL-22. Crucially, HQD promoted a shift in expression from the ISC marker Lgr5 toward differentiation markers MUC2, LYZ, and ChgA, indicating enhanced ISC differentiation and improved barrier function. These effects were effectively blocked by AhR inhibition or antibiotic treatment. CONCLUSION:HQD restores intestinal mucosal integrity and attenuates colonic inflammation by modulating gut microbiota composition, increasing microbial tryptophan metabolites with AhR-agonist activity, activating the AhR signaling pathway, and promoting ISC differentiation into functional epithelial cells. This work reveals a novel "microbiota-tryptophan metabolism-AhR-ISC differentiation" axis underlying HQD's therapeutic efficacy in UC.

BACKGROUND AND AIM:Huangqin decoction (HQD) is a Chinese medicine used to treat colitis and colorectal cancer (CRC). However, the specific compounds and mechanisms of HQD remain unclear despite its good curative clinical results. Through bioinformatics, network pharmacology, and experiments, this study aims to explore the progressive mechanisms of colitis-associated colorectal cancer (CAC) from ulcerative colitis (UC) while examining the protective effects of HQD and its compounds against this.METHODS:Bioinformatics was utilized to identify the hub genes between UC and CRC, and their clinical predictive significance, function, and expression were validated. Employing network pharmacology in combination with hub genes, key targets of HQD for preventing the development of UC into CAC were identified. Molecular docking and molecular dynamics (MD) were utilized to procure compounds that effectively bind to these targets and their transcription factors (TFs). Finally, the expression and mechanism of key targets were demonstrated in mice with UC or CAC.RESULTS:(1) Joint analysis of UC and CRC gene sets resulted in 14 hub genes, mainly related to extracellular matrix receptor binding, biological processes in the extracellular matrix, focal adhesion and neutrophil migration; (2) Network pharmacology results show HQD has 133 core targets for treating UC and CRC, acting on extracellular matrix, inflammatory bowel disease, chemical carcinogen receptor activation and other pathways; (3) The intersection of hub genes and core targets yielded two key targets, MMP1 and MMP3; (4) STAT3 is a shared TF of MMP1 and MMP3. (5) Molecular docking and MD verified that the dockings between Glabridin and STAT3/MMP1/MMP3 are stable and reliable; (6) In murine vivo experiments verified that Glabridin reduces inflammation, extracellular matrix degradation, and the occurrence of epithelial-mesenchymal transition to prevent UC transforming into CAC by inhibiting the phosphorylation of STAT3 and regulating the activity of MMP1/3.

This study aims to elucidate the mechanism of Huangqin Decoction(HQD)in treating ulcerative colitis(UC)by inves-tigating the relationship between tryptophan metabolism and intestinal barriers.In the in vivo experiments,3％dextran sulfate sodium(DSS)was used to induce a mouse model of acute colitis,with mesalazine as a positive control.The therapeutic effect of HQD on mice with UC was evaluated according to body weight,disease activity index(DAI),colon length,and pathological changes.Targeted metabolomics was used to detect the concentration of tryptophan and its metabolites in mouse feces.Western blot and RT-qPCR tech-niques were used to assess the expression levels of colonic aryl hydrocarbon receptor(AhR),myosin light chain kinase(MLCK),myo-sin light chain(MLC),and p-MLC.Serum FITC-dextran concentration,bacterial culture of mesenteric lymph nodes and spleen,as well as fluorescence probe in situ hybridization technique were used to evaluate intestinal epithelial permeability.Alcian blue and nu-clear fast red staining,Western blot,and RT-qPCR techniques were used to detect the expression of mucin secreted by the mouse's in-testinal epithelial goblet cells.Transmission electron microscopy was utilized to observe the connections of the mouse's intestinal epithe-lial cells.Immunofluorescence,Western blot,and RT-qPCR techniques were used to assess the expression of tight junction proteins in the mouse's intestinal epithelium.In the in vitro experiments,lipopolysaccharide(LPS)was used to induce intestinal epithelial barrier injury model in Caco2 cells,and AhR siRNA was used to further clarify the mechanism of HQD in activating AhR to improve intestinal barrier function.The results demonstrated that HQD effectively alleviated symptoms and pathological changes in the colon of DSS-in-duced mice with colitis.Treatment with HQD could regulate tryptophan metabolism in the feces of mice with colitis,activate AhR,and improve the intestinal epithelial barrier.Additionally,the results of the in vitro experiments confirmed that HQD could restore the ex-pression of tight junction proteins in the intestinal epithelium of colitis cells by activating AhR to regulate the MLCK/p-MLC signaling pathway.

目的 了解疫情期间高校医学生对网络课程的满意度。方法 以临床医学、口腔医学和康复治疗学专业学生为调查对象，开展问卷调查。结果 学生对本次网络课程总体满意度较高，其中对学习效果、课程内容及教学条件方面的满意度均较高，但对学习能力的培养及提高学习兴趣方面的满意度欠佳。结论 为提高学生在疫情环境下，对网络课程的满意度，应丰富网络教学资料，完善和提高教学手段。

In recent years, hydrogel microsphere has attracted much attention due to its great potential in the field of skin repair. This paper reviewed the recent progress in the preparation strategy of hydrogel microsphere and its application in skin repair. In this review, several preparation methods of hydrogel microsphere were summarized in detail. In addition, the related research progress of hydrogel microspheres for skin repair was reviewed, and focused on the application of bioactive microspheres, antibacterial microspheres, hemostatic microspheres, and hydrogel microspheres as delivery platforms (hydrogel microspheres as a microcarrier of drugs, bioactive factors, or cells) in the field of skin repair. Finally, the limitations and future prospects of the development of hydrogel microspheres and its application in the field of skin repair were presented. It is hoped that this review can provide a valuable reference for the development of the preparation strategy of hydrogel microspheres and promote the application of hydrogel microspheres in skin repair.

Aims: Endoplasmic reticulum stress (ER stress) plays an important role in podocyte injury in diabetic nephropathy. Wnt/β-catenin signaling modulates ER stress, yet the epigenetic regulation of β-catenin in ER stress and podocyte injury remains largely unknown. Herein, we tested the hypothesis that LINC00355 recruits EZH1 to the promoter region of CTNNBIP1 and trimethylates H3K4 to regulate ER-stress induced podocyte injury in DN. Results: LINC00355 is upregulated in podocytes and correlates with renal function decline in DN patients. LINC00355 localizes in the nucleus and exerts biological functions by directly binding EZH1, which epigenetically targets CTNNBIP1 through repressive trimethylation of H3K4 and activates Wnt/β-catenin signaling and ER stress. Further, we provide mechanistic evidences that LINC00355 recruits EZH1 to the promoter region of CTNNBIP1 and regulates ER-stress induced podocyte injury in DN. Innovation and Conclusion: Our data reveal a major role of LINC00355/EZH1/CTNNBIP1 network in triggering podocyte injury, providing new evidences for understanding the role of ER stress in DN. Antioxid. Redox Signal. 39, 225-240.

目的 分析和探讨A大学疫情防控开始期间教师对网络教学活动的满意度及面临的问题与挑战，并提出提升高校网络教学质量的改进对策。方法 对学校教师进行问卷调查，共回收196份教师有效问卷，对问卷进行分析。结果 总体来看，62.24%的教师对对新的教学方法（如PBL、慕课、混合式教学等）不够了解，48.98%的教师对网络教学与传统教学的主要区别不够了解；69.89%教师持乐观态度，只有5.61%的教师对网络教学比较悲观，认为可能不利于教学开展；32.65%的教师对学校网络教学相关制度的规定不满意，超过一半的教师认为相关制度存在制度不够系统和细化、内容不够完善、存在执行程序繁琐的问题。结论 教师对网络教学持积极态度，但是对网络教学了解不够。教师要从自身出发，积极学习各种网络教学平台的使用方法。学校应积极举办网络教学技术方面的科普、培训会议、加大对网络教学资金的投入，健全网上教学监管制度。

Abstract Background Prostate cancer (PCa), an inert tumour, has a long progression period, but valid biomarkers and methods for effectively and sensitively monitoring PCa progression are lacking, prompting us to identify new predictors for diagnosis and prognosis. Posttranslational modifications characterizing receptor activation are considered potentially strong indicators of disease progression. Methods The posttranscriptional regulation of leukaemia inhibitory factor receptor (LIFR) and its novel downstream signalling activity in PCa were studied using liquid mass spectrometry, genetically engineered mouse (GEM) models, organoid assays, lentivirus packaging, infection and stable cell line construction. Results In this study, the level of acetylated K620 on LIFR in its extracellular domain was shown to predict the progression and prognosis of PCa. In PCa cells, LIFR‐K620 acetylation is reversibly mediated by GCN5 and SIRT2. GEM experiments and organoid assays confirmed that the loss of LIFR‐K620 acetylation inhibits PCa progression. Mechanistically, K620 acetylation facilitates LIFR homodimerization and subsequently promotes LIFR‐S1044 phosphorylation and activation, which further recruits PDPK1 to activate AKT signalling and sequentially enhances the GCN5 protein level to sustain the protumour level of LIFR‐K620 acetylation by preventing GCN5 degradation via CRL4Cdt2 E3 ligase. Conclusions Acetylation of extracellular K620 on LIFR reinforces its homodimerization and integrates the activities of PDPK1, AKT, GSK3β and GCN5 to form a novel positive feedback loop in PCa; this modification is thus a promising biomarker for monitoring PCa progression.

Shaoyao decoction (SYD), a classical traditional Chinese medicine formula, is effective for the treatment of inflammatory bowel disease (IBD). This study was designed to investigate the therapeutic effects of SYD on IBD and possible mechanisms. Dextran sulfate sodium (DSS, 3.5%) was used to induce colitis in C57BL/6 mice. Disease phenotypes were investigated based on disease activity index (DAI), colon length, and microscopic and macroscopic scores. Additionally, the presence of proinflammatory cytokines, immune cell infiltrates, intestinal cell proliferation, apoptosis, epithelial permeability, signal transducer and activator of transcription 3 (STAT3), and nuclear factor-κB (NF-κB) signaling, as well as the intestinal mucosal barrier function, were investigated. The administration of SYD significantly ameliorated the clinical signs, suppressed the levels of proinflammatory cytokines, and reduced immune cell infiltrates into colonic tissues of DSS-induced colitis model mice. SYD also significantly reduced the DSS-induced activation of STAT3 and NF-κB signaling. Furthermore, SYD promoted epithelial integrity by regulating epithelial cell apoptosis and epithelial permeability. Finally, we demonstrated that SYD protected the intestinal barrier function by significantly regulating the mucus layer genes Muc1 , Muc2 , Muc4 , and Tff3 , as well as the epithelial barrier genes Z O -1 and Occludin . Our results indicate that SYD has a protective effect on DSS-induced colitis, which is attributable to its anti-inflammatory activity and intestinal barrier function-enhancing effects. These results provide valuable insights into the pharmacological actions of SYD for the treatment of IBD.

OBJECTIVE:To explore the effect of Huangqin decoction (HQD) on group 3 innate lymphoid cells (ILC3s) and helper T cells (Th) for treatment of ulcerative colitis (UC).OBJECTIVE:Male Balb/c mice were randomly divided into control group, DSS group, mesalazine group (ME, 400 mg/kg), and 2.275 g/kg, 4.55 g/kg and 9.1 g/kg HQD groups. All the mice were given free access to normal chow. Except for those in the normal control group, all the mice were given 3% DSS solution for 7 days to establish models of UC. The mice in ME group and 3 HQD groups were given mesalazine or HQD via oral gavage at the specified doses once a day. Flow cytometry was performed to analyze the ILC3s, MHC Ⅱ, Th1 and Treg in the lamina propria lymphocytes in the colon. Milliplex was performed to determine cytokine levels of in the colon tissues.OBJECTIVE:Compared with those in DSS group, the mice in the 3 HQD groups all showed obviously lessened symptoms of UC with significantl decreased DAI score (P < 0.001) and macroscopic score (P < 0.001). The results of flow cytometry showed that HQD treatment significantly increased the percentage of ILC3s (P < 0.05) and expression of MHCⅡ (P < 0.05), obviously reduced the proportion of Th1 (P < 0.05) but increased Treg cells (P < 0.05) in the colon tissues. Milliplex showed that HQD treatment significantly reduced the expressions of Th-related pro-inflammatory cytokines including IL-2 (P < 0.05), IL-17A (P < 0.05), IL-23 (P < 0.05), TNF-α (P < 0.05), and IFN-γ (P < 0.05).OBJECTIVE:HQD alleviates DSS- induced UC in mice by increasing ILC3s and MHC Ⅱ expression to suppress the function of Th17 and Th1 cells and promote Treg and Th2 cells.

目的 在常规使用降压药物治疗的基础上,探讨应用中药沐足治疗原发性高血压伴失眠患者睡眠质量的影响.方法 选取东莞市寮步医院2019年12月至2021年1月收治的120例原发性高血压伴失眠患者作为研究对象,采用随机数字表法将患者分为对照组和观察组,每组60例.两组患者均给予常规西药和柴胡加龙骨牡蛎汤加减干预治疗,观察组在此基础上配合中药沐足,治疗时间均为8周.比较两组患者治疗前后的血压、睡眠质量评分、中医证候积分及临床疗效.结果 治疗8周后对照组和观察组患者的血压、匹茨堡睡眠质量指数(PSQI)评分及中医证候积分均有效降低(P<0.05).治疗8周后,观察组患者血压、PSQI评分及中医证候积分均低于对照组,差异有统计学意义(P<0.05).观察组总有效率为93.33％,对照组为80.00％,两组比较差异有统计学意义(P<0.05).结论 在常规中西医结合治疗基础上,配合中药沐足,不仅可以降低原发性高血压伴失眠患者的血压水平,减轻临床症状,还可以改善患者的睡眠质量,疗效显著,值得进一步推广.

目的 基于STAT3/Bcl-2信号通路探究黄芩苷对人结肠癌SW480细胞增殖和凋亡的影响.方法 实验分为空白组及黄芩苷25,50,100,200,400μg/mL组,空白组用不含黄芩苷Gibco RPMI 1640培养基培养,黄芩苷各组采用相应浓度黄芩苷培养,分别处理结肠癌SW480细胞24 h后,采用CCK-8法、Edu染色法、Annexin V-FITC/PI法检测经上述处理细胞的增殖和凋亡情况,采用Western blot法检测人结肠癌SW480细胞中促进凋亡相关蛋白Bax、Caspase-3和抑制凋亡相关蛋白Bcl-2以及转录相关蛋白STAT-3的表达情况.结果 黄芩苷各组的细胞增殖率均明显低于空白组(P均<0.05),且细胞增殖率随着黄芩苷浓度的增高而缓慢下降,当黄芩苷浓度达400μg/mL时,增殖率下降1/4;人结肠癌SW480细胞凋亡率有随着黄芩苷浓度的增加而逐渐升高的趋势.随着黄芩苷浓度的增加,Bax蛋白表达量逐渐增加,黄芩苷100,200,400μg/mL组明显高于空白组(P均<0.05),但黄芩苷200μg/mL和400μg/mL组比较差异无统计学意义(P>0.05);STAT-3和Bcl-2蛋白表达量逐渐降低,黄芩苷50,100,200,400μg/mL组均明显低于空白组(P均<0.05);黄芩苷50,100,200,400μg/mL组Caspase-3蛋白表达量呈下降趋势,但与空白组比较差异均无统计学意义(P均>0.05).结论 黄芩苷能诱导人结肠癌SW480细胞凋亡并抑制其增殖,且与黄芩苷浓度呈一定的量效关系,其机制可能与调节STAT3/Bcl-2通路有关.

Introduction. It has been reported that the traditional Chinese medicine Huangqin-Tang decoction (HQT) has a protective effect on the epithelial barrier function of ulcerative colitis, but its mechanism has not been fully clarified. This study intends to explore the protective mechanism of HQT in regulating microRNA (miRNA) for the first time. Methods. Based on the Balb/c mice ulcerative colitis model, the mice were given a gavage of 0.1 mL/10 g HQT every day for 7 days; on the 8th day, the colon of the mice was dissected, the length of the colon for the mice was measured, and the score was given based on this. Analysis of colonic mucosal injury was conducted by hematoxylin-eosin staining. Then, the differential miRNA was screened and sequenced in colon tissue using the HiSeq platform. And the differential miR-185-3p gene was verified by RT-PCR. Finally, the effects of HQT on miR-185-3p, occludin protein expression, and transepithelial electrical resistance (TEER) value were observed in combination with the CaCo2 intestinal epithelial cell model. Results. HQT treatment can alleviate the shortening of colon length and reverse the intestinal mucosal injury. miRNA sequencing of colonic tissue showed that miR-185-3p was significantly downregulated in the model group, while HQT could upregulate miR-185-3p, thereby affecting the myosin light chain kinase (MLCK)/myosin light chain phosphorylation (p-MLC) pathway and leading to increased expression of occludin protein, which ultimately protected the intestinal epithelial barrier function. Conclusion. HQT can protect colon epithelial barrier function by regulating miR-185-3p.

Although several clinical trials studied the efficacy of chitosan on weight loss, controversial results have been found. Herein, we evaluated randomized controlled trials (RCTs) of chitosan consumption in adult participants on body weight and body composition through a meta-analysis with trial sequential analysis (TSA). We searched EMBASE, MEDLINE, Web of Science, and CENTRAL databases. The primary body composition indices including body weight, body mass index (BMI), waist circumference, body fat, and hip circumference were extracted. The quality of included articles was assessed according to the Cochrane risk of bias tool. Data were pooled using the random-effects models and calculated as weighted mean difference (WMD) with 95% confidence intervals (CI). Heterogeneity investigated using I-2 statistics. TSA, subgroup analyses, sensitivity analysis, meta-regression and publication bias were also evaluated. Overall, 15 eligible trials (18 treatment arms) with 1130 subjects were included. The pooled analyses revealed a significant reduction in body weight (WMD, -0.89 kg; 95% CI, -1.41 to -0.38; P = 0.0006), BMI (WMD, -0.39 kg/m(2); 95% CI, -0.64 to -0.14; P = 0.002) and body fat (WMD, -0.69%; 95% CI, -1.02 to -0.35; P = 0.0001) receiving chitosan supplementation. Subgroup analyses also showed that consuming chitosan in dose (>2.4 g/d), shorter-term (<12 weeks), studies with parallel design and studies including participants with obese or overweight had positive effects on body composition. TSA provided conclusive evidence for the benefit of chitosan supplementation. Our findings provided evidence that chitosan consumption might be a useful adjunctive pharmacological therapeutic tool for body weight management particularly in overweight/obese participants. Further well-constructed clinical trials that target body weight and body composition as their primary outcomes are needed.

Morinda officinalis F.C. How. (Rubiaceae) is a herbal medicine. It has been recorded that its oligosaccharides have neuroprotective properties. In order to understand the oligosaccharides extracted from Morinda officinalis (OMO), a systematic study was conducted to provide evidence that supports its use in neuroprotective therapies for Alzheimer’s disease (AD). AD rat models were prepared with D-galactose and Aβ25–35. The following groups were used in the present experiment: normal control group, sham-operated group, model group, Aricept group, OMO low-dose group, OMO medium-dose group, and OMO high-dose group. The effects on behavioral tests, antioxidant levels, energy metabolism, neurotransmitter levels, and AD-related proteins were detected with corresponding methodologies. AD rats administered with different doses of OMO all exhibited a significant (P<0.05) decrease in latency and an increase (P<0.05) in the ratio of swimming distance to total distance in a dose-dependent manner in the Morris water maze. There was a significant (P<0.05) increase in antioxidant enzyme activities (SOD, GSH-Px, and CAT), neurotransmitter levels (acetylcholine, γ-GABA, and NE and DA), energy metabolism (Na+/K+-ATPase), and relative synaptophysin (SYP) expression levels in AD rats administered with OMO. Furthermore, there was a significant (P<0.05) decrease in MDA levels and relative expression levels of APP, tau, and caspase-3 in AD rats with OMO. The present research suggests that OMO protects against D-galactose and Aβ25–35-induced neurodegeneration, which may provide a novel strategy for improving AD in clinic.

Janus激酶/信号传导与转录激活子(Janus kinase/signal transduction and activator of transcription,JAK/STAT)信号通路是众多细胞因子信号传导的共同途径,不同程度地参与细胞增殖、分化、凋亡及炎症等过程,进而促进各种疾病的发生、发展,包括炎症性肠病(inflammatory bowel disease,IBD).IBD是一种肠道慢性非特异性炎症疾病,常反复发作且病因不明.我们通过探讨JAK/STAT信号传导结构及其促成IBD发病的相关机制,并就JAK抑制剂在JAK/STAT信号通路在IBD现在和未来的治疗方法 中的应用作一概述.

Diabetic nephropathy (DN) is the leading cause of end-stage kidney disease. TGF-beta 1/Smad3 signalling plays a major pathological role in DN; however, the contribution of Smad4 has not been examined. Smad4 depletion in the kidney using anti-Smad4 locked nucleic acid halted progressive podocyte damage and glomerulosclerosis in mouse type 2 DN, suggesting a pathogenic role of Smad4 in podocytes. Smad4 is upregulated in human and mouse podocytes during DN. Conditional Smad4 deletion in podocytes protects mice from type 2 DN, independent of obesity. Mechanistically, hyperglycaemia induces Smad4 localization to mitochondria in podocytes, resulting in reduced glycolysis and oxidative phosphorylation and increased production of reactive oxygen species. This operates, in part, via direct binding of Smad4 to the glycolytic enzyme PKM2 and reducing the active tetrameric form of PKM2. In addition, Smad4 interacts with ATPIF1, causing a reduction in ATPIF1 degradation. In conclusion, we have discovered a mitochondrial mechanism by which Smad4 causes diabetic podocyte injury.

目的 探讨白细胞介素22(IL-22)基因单核苷酸多态性与结直肠癌易感性和临床病理参数的相关性.方法 选取结直肠癌患者306例,健康对照者358例,采用TaqMan探针技术,对IL-22基因两个SNP位点(rs2227473和rs2227483)进行基因分型,统计分析结直肠癌患者和健康对照者的基因频率,并结合结直肠癌患者不同的临床特点、病理特征进行分层比较.结果 IL-22基因rs2227473位点在结直肠癌患者中G的等位基因频率为92％,在健康对照者中的等位基因频率为85.6％,差异具有统计学意义(x2=13.25,P=0.000 3);在临床分期中,rs2227473位点G的在Ⅰ+Ⅱ期患者中的基因频率为80.3％,在Ⅲ+Ⅳ期患者中的基因频率为91.5％,差异具有统计学意义(X2=16.7,P＜0.000 1).而rs2227473位点的基因型与血清癌胚抗原(CEA)、原发肿瘤扩展情况、淋巴结状态和转移情况的参数之间无显著相关性.且rs2227483位点的基因型及等位基因频率分布在结直肠癌患者与健康对照者间差异有统计学意义.结论 IL-22基因rs2227473多态性与结直肠癌的易感性和临床分期相关,其中携带等位基因G增加结直肠癌的发生风险.

The aim of this paper was to investigate the effect of Shaoyao Tang on ulcerative colitis(UC) in rats via regulation of TLR4/NF-κB signal pathway. A total of 56 Wistar rats were randomly divided into 6 groups: normal control group(double distilled water), model group(double distilled water), mesalazine group(10 mL·kg~(-1)), high dose, middle dose and low dose Shaoyao Tang groups(2.4, 1.2, and 0.6 g·mL~(-1)). After UC rat models were established by 2, 4-dinitrochlorobenzene(DNCB)/ethanol enema, the rats received double distilled water or corresponding drugs twice a day for 7 days. After the treatment cycle, the general performance and disease activity index(DAI) of rats were observed on the next day. Then the rats were sacrificed. The length of colon was measured. Macroscopic and histological score of colon were evaluated. Histopathological changes of colon were observed by HE staining. Ultraviolet spectrophotometry detection was used to detect the content of myeloperoxidase(MPO) in blood and colon tissues. The levels of P-selectin, macrophage migration inhibitory factor(MIF) and thromboxane B_2(TXB_2) in blood and colon tissues were determined by ELISA. Immunohistochemistry and Western blot analysis were performed to detect the protein expressions of TLR4 and NF-κB in colon tissues. The results showed that as compared with the model group, Shaoyao Tang of different doses improved the general performance of UC rats. Moreover, high-dose Shaoyao Tang group showed the most obvious effect in scoring of disease activity index(P<0.001); both medium and high doses of Shaoyao Tang significantly inhibited the colon shortening and pathological injury, with significantly decreased expression levels of MPO, P-selectin, MIF and TXB_(2 )in serum and colon tissues of UC rats(P<0.001). Immunohistochemistry and Western blot assay showed that the levels of TLR4 and NF-κB protein expression in the colon tissues of Shaoyao Tang high-dose group were remarkably lower than that in the model group(P<0.001). This study shows that Shaoyao Tang has protective and repairing effects on UC, and its possible mechanism is achieved probably by regulating the TLR4/NF-κB pathway and inhibiting the expressions of MPO, P-selectin, MIF and TXB_2.