Improvement of Phased Antenna Array Applied in Focused Microwave Breast Hyperthermia.

Focused microwave breast hyperthermia (FMBH) employs a phased antenna array to perform beamforming that can focus microwave energy at targeted breast tumors. Selective heating of the tumor endows the hyperthermia treatment with high accuracy and low side effects. The effect of FMBH is highly dependent on the applied phased antenna array. This work investigates the effect of polarizations of antenna elements on the microwave-focusing results by simulations. We explore two kinds of antenna arrays with the same number of elements using different digital realistic human breast phantoms. The first array has all the elements' polarization in the vertical plane of the breast, while the second array has half of the elements' polarization in the vertical plane and the other half in the transverse plane, i.e., cross polarization. In total, 96 sets of different simulations are performed, and the results show that the second array leads to a better focusing effect in dense breasts than the first array. This work is very meaningful for the potential improvement of the antenna array for FMBH, which is of great significance for the future clinical applications of FMBH. The antenna array with cross polarization can also be applied in microwave imaging and sensing for biomedical applications.

Validation of mitochondrial biomarkers and immune dynamics in polycystic ovary syndrome.

PROBLEM: Polycystic ovary syndrome (PCOS), a prevalent endocrine-metabolic disorder, presents considerable therapeutic challenges due to its complex and elusive pathophysiology. METHOD OF STUDY: We employed three machine learning algorithms to identify potential biomarkers within a training dataset, comprising GSE138518, GSE155489, and GSE193123. The diagnostic accuracy of these biomarkers was rigorously evaluated using a validation dataset using area under the curve (AUC) metrics. Further validation in clinical samples was conducted using PCR and immunofluorescence techniques. Additionally, we investigate the complex interplay among immune cells in PCOS using CIBERSORT to uncover the relationships between the identified biomarkers and various immune cell types. RESULTS: Our analysis identified ACSS2, LPIN1, and NR4A1 as key mitochondria-related biomarkers associated with PCOS. A notable difference was observed in the immune microenvironment between PCOS patients and healthy controls. In particular, LPIN1 exhibited a positive correlation with resting mast cells, whereas NR4A1 demonstrated a negative correlation with monocytes in PCOS patients. CONCLUSION: ACSS2, LPIN1, and NR4A1 emerge as PCOS-related diagnostic biomarkers and potential intervention targets, opening new avenues for the diagnosis and management of PCOS.

Uncovering the potential of APOD as a biomarker in gastric cancer: A retrospective and multi-center study.

Gastric cancer (GC) poses a significant health challenge worldwide, necessitating the identification of predictive biomarkers to improve prognosis. Dysregulated lipid metabolism is a well-recognized hallmark of tumorigenesis, prompting investigation into apolipoproteins (APOs). In this study, we focused on apolipoprotein D (APOD) following comprehensive analyses of APOs in pan-cancer. Utilizing data from the TCGA-STAD and GSE62254 cohorts, we elucidated associations between APOD expression and multiple facets of GC, including prognosis, tumor microenvironment (TME), cancer biomarkers, mutations, and immunotherapy response, and identified potential anti-GC drugs. Single-cell analyses and immunohistochemical staining confirmed APOD expression in fibroblasts within the GC microenvironment. Additionally, we independently validated the prognostic significance of APOD in the ZN-GC cohort. Our comprehensive analyses revealed that high APOD expression in GC patients was notably associated with unfavorable clinical outcomes, reduced microsatellite instability and tumor mutation burden, alterations in the TME, and diminished response to immunotherapy. These findings provide valuable insights into the potential prognostic and therapeutic implications of APOD in GC.

Causal Relationship between Immune Cells and Gynecological Cancers through Bidirectional and Multivariable Mendelian Randomization Analyses.

Background: Evidence suggests potential associations between gynecological malignancies and various immune cell chemicals and systems. However, establishing a causal relationship remains uncertain. Methods: This work employed Wald ratio for one single-nucleotide polymorphism (SNP) or the inverse-variance weighted method (IVW) for multiple SNPs to conduct bidirectional two-sample Mendelian randomization (MR) analysis by utilizing genome-wide association study (GWAS) data. We employed supplementary methods, including MR-Egger and weighted median methods, to detect and correct for the influence of horizontal pleiotropy. In addition, we also use colocalization analysis for further validation. Results: In IVW analysis, increases in relative count of circulating CD11c+ HLA-DR++ conventional dendritic cells (cDC) were associated with an elevated risk of breast cancer (OR [95% CI], 1.1295 [1.0632-1.2000], P = 8.044 × 10-5), while elevated levels of HLA-DR on plasmacytoid dendritic cells (DC) and HLA-DR on DC were protective against breast cancer. In addition, actual count of CD39+ resting Treg AC was also shown to be causally associated with the development of ovarian cancer, whereas a high relative count of CD28+ CD45RA- CD8+ T cells reduced the risk of cervical cancer. Sensitivity analysis revealed almost no evidence of bias in the current study. Multivariable MR (MVMR) analyses further confirmed a direct impact of the CD11c+ HLA-DR++ cDC immune phenotype on breast cancer. Colocalization analysis showed the lead SNP, rs780094, suggesting HLA-DR GWAS shared a common genetic mechanism with breast cancer. Conclusions: The MR study identified significant causal relationships between multiple immunophenotypes and breast cancer, aiming to provide clinicians with some reference for cancer prediction and explore further potential associations between immune phenotypes and gynecologic tumors.

Structurally manipulated antioxidant peptides derived from wheat bran: Preparation and identification.

Bioactive peptide's development is facing two challenges in terms of its lower yield and limited understanding of structurally orientated functionality. Therefore, peptides were prepared from wheat bran via a cocktail enzyme for achieving a higher level of hydrophobic amino acids than traditional method. The obtained peptides exhibited great antioxidant activities against H2O2-induced oxidative stress in HepG2 cells. Among them, 91 bioactive peptides were selected through the virtual screening, and their N-terminal and C-terminal contained many hydrophobic amino acids. Then the peptides with capacity to interact with Keap1 were identified by in silico simulation, because Keap1 acts as a sensor of redox insults. The results revealed that peptides DLDW and DLGL demonstrated the highest binding affinities, and a bridge was formed between Asp of DLGL and Arg415 of Klech domain, contributing to interfering Keap1-Nrf2 interaction. These findings implied a potential application of wheat bran peptides as nutraceuticals and health-promoting ingredients.

An "AND" Logic-Gated Prodrug Micelle Locally Stimulates Antitumor Immunity.

Materials that can respond to multiple biomarkers simultaneously, acting as an "AND" gate, have the potential to enhance tumor-targeting for drug delivery. In this study, an "AND" logic-controlled release prodrug micelle is developed for codelivering the chemotherapeutic and the stimulator of interferon genes (STING) agonist, enabling precise combinatorial therapy. The drug release is programmed by tumor-enriched boramino acids (BAA) in the tumor microenvironment and intracellular reactive oxygen species (ROS), resulting in enhanced tumor targeting. STING agonist is successfully encapsulated into prodrug micelles through π-π stacking and hydrophobic interactions. These AND logic-gated prodrug micelles can achieve tumor-targeted delivery of STING agonist, leading to significantly enhanced immune activation and antitumor efficacy in vivo. It is expected that this clinically relevant nanoplatform will provide a rational design of an effective immunotherapy combination regimen to convert immunologically "cold" tumors to immunogenic "hot" tumors, addressing the major challenges faced by immunotherapies.

Pan-cancer analysis revealing that PTPN2 is an indicator of risk stratification for acute myeloid leukemia.

The non-receptor protein tyrosine phosphatases gene family (PTPNs) is involved in the tumorigenesis and development of many cancers, but the role of PTPNs in acute myeloid leukemia (AML) remains unclear. After a comprehensive evaluation on the expression patterns and immunological effects of PTPNs using a pan-cancer analysis based on RNA sequencing data obtained from The Cancer Genome Atlas, the most valuable gene PTPN2 was discovered. Further investigation of the expression patterns of PTPN2 in different tissues and cells showed a robust correlation with AML. PTPN2 was then systematically correlated with immunological signatures in the AML tumor microenvironment and its differential expression was verified using clinical samples. In addition, a prediction model, being validated and compared with other models, was developed in our research. The systematic analysis of PTPN family reveals that the effect of PTPNs on cancer may be correlated to mediating cell cycle-related pathways. It was then found that PTPN2 was highly expressed in hematologic diseases and bone marrow tissues, and its differential expression in AML patients and normal humans was verified by clinical samples. Based on its correlation with immune infiltrates, immunomodulators, and immune checkpoint, PTPN2 was found to be a reliable biomarker in the immunotherapy cohort and a prognostic predictor of AML. And PTPN2'riskscore can accurately predict the prognosis and response of cancer immunotherapy. These findings revealed the correlation between PTPNs and immunophenotype, which may be related to cell cycle. PTPN2 was differentially expressed between clinical AML patients and normal people. It is a diagnostic biomarker and potentially therapeutic target, providing targeted guidance for clinical treatment.

Cordycepin inhibits myogenesis via activating the ERK1/2 MAPK signalling pathway in C2C12 cells.

Cordycepin (with a molecular formula of C10H13N5O3), a natural adenosine isolated from Cordyceps militaris, has an important regulatory effect on skeletal muscle remodelling and quality maintenance. The aim of this study was to investigate the effect of cordycepin on myoblast differentiation and explore the underlying molecular mechanisms of this effect. Our results showed that cordycepin inhibited myogenesis by downregulating myogenic differentiation (MyoD) and myogenin (MyoG), preserved undifferentiated reserve cell pools by upregulating myogenic factor 5 (Myf5) and retinoblastoma-like protein p130 (p130), and enhanced energy reserves by decreasing intracellular reactive oxygen species (ROS) and enhancing mitochondrial membrane potential, mitochondrial mass, and ATP content. The effect of cordycepin on myogenesis was associated with increased phosphorylation of extracellular signal-regulated kinase 1/2 (p-ERK1/2). PD98059 (a specific inhibitor of p-ERK1/2) attenuated the inhibitory effect of cordycepin on C2C12 differentiation. The present study reveals that cordycepin inhibits myogenesis through ERK1/2 MAPK signalling activation accompanied by an increase in skeletal muscle energy reserves and improving skeletal muscle oxidative stress, which may have implications for its further application for the prevention and treatment of degenerative muscle diseases caused by the depletion of depleted muscle stem cells.

Chemical characterization, antioxidant and immunomodulatory activities of acetylated polysaccharides from Cyperus esculentus.

This research was designed to characterize the structure of Cyperus esculentus polysaccharide (CEP) and its acetylated one (ACEP), and then investigated the effects of acetylation on the changes in physicochemical properties, thermal stability, antioxidant and immunomodulatory activities. Results showed that CEP and ACEP were heteropolysaccharides consisting of glucose, mannose, arabinose and xylose. The main chain of CEP included α-1,4-Glcp residues with the branching points at the O-6 position of the α-1,6-Manp residues. Acetyl groups were substituted at the O-2 and O-6 positions of some glucose residues. Meanwhile, the acetylation remarkably improved the polysaccharides thermal stability, and the ACEP exhibited a greater antioxidant activity. Furthermore, CEP and ACEP were proved to protect RAW 264.7 cells against LPS-induced inflammation by improving cellular morphology and decreasing reactive oxygen species secretion. This study may highlight a new approach for developing a high value-added ingredient from C. esculentus for functional food industry.

[Interleukin 34 (IL-34) promotes the proliferation and odontogenic differentiation of rat apical papillary stem cells].

Objective To investigate the effect of interleukin-34 (IL-34) on the odontogenic and osteogenic differentiation of stem cells from the apical papilla (SCAPs) in rats. Methods SCAPs were isolated and cultured by enzyme digestion method, and the expression of IL-34 in SCAPs was detected by real-time fluorescence quantitative PCR(RT-PCR). MTT assay was used to analyze the effects of different concentrations of IL-34 on SCAPs' proliferation in rats. The mineralization was observed by alizarin red staining, and the proliferation capacity was detected by scratch test. The expressions of alkaline phosphatase (ALP), dentin sialophosphoprotein (DSPP), runt-related transcription factor 2 (Runx2) and critical transcription factor osterix (OSX) were detected by RT-PCR. The protein expressions of ALP, DSPP, Runx2 and OSX were detected by Western blot analysis. Results The maximum concentration of IL-34 promoting the proliferation of SCAPs in rats was 100 ng/mL. Aalizarin red staining showed that IL-34 could promote the mineralization of SCAPs. RT-PCR and Western blot analysis showed that 100 ng/mL IL-34 could promote the expression of ALP, DSPP, Runx2 and OSX. Conclusion IL-34 can promote the proliferation and odontogenic/osteogenic differentiation of SCAPs in rats.

Valproic acid regulates MIEF1 through MST2-HIPPO to suppress breast cancer growth.

AIMS: To determine the effects of valproic acid (VPA) on anti-proliferative effects and mitochondrial function in breast cancer cells and the underlying mechanisms involved in the effects, with a focus on signal transduction. MAIN METHODS: The inhibitory effect of valproic acid on breast cancer in vivo and in vitro was evaluated by cellular and animal experiments. Mitochondria-related proteins as well as hippo pathway were monitored by western blotting. The effects of VPA on mitochondrial membrane potential, reactive oxygen species, and apoptosis were confirmed by flow cytometry. In addition, the involvement of hippo pathway in the regulation of mitochondrial function by VPA was verified by XMU-MP-1 (MST2 inhibitor). KEY FINDINGS: In this study, we highlight that VPA significantly attenuates mitochondrial function, leading to inhibited cell proliferation and reduced colony formation in MCF-7 and MDA-MB-231 breast cancer cells. Mechanistically, VPA-induced suppression of mitochondrial aerobic respiration was mediated by decreased expression of mitochondrial elongation factor 1 through activation of the hippo pathway, resulting in impaired breast cancer growth. In summary, we uncover a novel mechanism of VPA in regulating mitochondrial aerobic respiration, which is essential for developing an effective approach in breast cancer therapy. SIGNIFICANCE: Mitochondrial aerobic respiration and its products are the main sources of energy for tumors; therefore, studying the role of mitochondrial function in tumor cells is significant. VPA has been used as a therapeutic agent for cancer. However, the detail mechanism underlying the effects of VPA on mitochondrial function in breast cancer remains unclear.

Cancer Risk in Hashimoto's Thyroiditis: a Systematic Review and Meta-Analysis.

Objective: Research data suggest that patients with Hashimoto's thyroiditis may increase the risk of cancer. However, existing research is inconsistent with this view. Therefore, to investigate the effect of Hashimoto's thyroiditis on the risk of developing cancer, we conducted this study. Methods: We searched the PubMed and Embase databases from database establishment until March 2022. After rigorous literature screening by two authors, 23 studies that met the inclusion criteria were identified, and the required data were independently extracted. Results: We retrieved 3591 records, and after the screening, 11 case-control studies and 12 cohort studies were included in the analysis. Data analysis suggested that patients with Hashimoto's thyroiditis had an increased risk of developing breast cancer, urogenital cancer, digestive organs cancer, hematologic cancer, and a low risk of respiratory cancers. Conclusions: This systematic review and meta-analysis showed that patients with HT may have a significantly increased risk of thyroid cancer, breast cancers, lung cancer, digestive system cancer, urogenital cancers, blood cancers, and prolactinoma people without HT. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/, identifier CRD 42022320741.

miRNA-877-5p inhibits malignant progression of prostate cancer by directly targeting SSFA2.

In this study, we aimed to investigate the role of miR-877-5p in the malignant phenotypes of prostate cancer (PCa) cells and its underlying mechanism. RT-qPCR analysis was performed to examine the expression of miR-877-5p and sperm-specific antigen 2 (SSFA2) in PCa tissues and cells. Cell counting kit-8 (CCK-8) assay, 5-ethynyl-20-deoxyuridine (EdU) assay, flow cytometry, wound-healing assay, and Transwell invasion assay were performed to determine the functional roles of miR-877-5p in PCa cells. The association of miR-877-5p with SSFA2 was determined by luciferase reporter and RNA pull-down assays. In this study, we found that the expression level of miR-877-5p was decreased in PCa tissues and cells. Functionally, overexpression of miR-877-5p exerted tumor suppressor properties in PCa cells. Mechanistically, SSFA2 was identified as a target gene of miR-877-5p, while overexpression of SSFA2 could abrogate the anti-tumor effects of miR-877-5p in PCa cells. These findings demonstrated that miR-877-5p/SSFA2 axis functioned as a potential target for PCa treatment.

pH-Sensitive Polycations for siRNA Delivery: Effect of Asymmetric Structures of Tertiary Amine Groups.

pH-sensitive polyelectrolytes provide enormous opportunity for siRNA delivery. Especially, their tertiary amine structures can not only bind genes but also act as pH-sensitive hydrophobic structure to control genes release. However, the influence of molecular structures on siRNA delivery still remains elusive, especially for the asymmetric alkyl substituents of the tertiary amine groups. Herein, a library of N-methyl-N-alkyl aminoethyl methacrylate monomers (MsAM) with asymmetric alkyl substituents on the tertiary amine group is synthesized and used to prepare a series of tri-block polycationic copolymers poly(aminoethyl methacrylate)-block-poly (N-methyl-N-alkyl aminoethyl methacrylate)-block-poly(ethylene glycol methacrylate) (PAMA-PMsMA-PEG). And the properties of these polycations and their self-assembled micelles are characterized, including molecular structure, proton buffering capacity, pH-sensitivity, size, and zeta potential. With the length increase of one alkyl substituent, the proton buffering capacity of both monomers and polycations is demonstrated to be narrowed down. The siRNA delivery efficiency and cytotoxicity of these micelles are also evaluated on HepG2 cells. In particular, poly(aminoethyl methacrylate)-block-poly(N-methyl-N-ethyl aminoethyl methacrylate)-block-poly(ethylene glycol methacrylate) (PAMA-PMEMA-PEG) elicited the best luciferase knockdown efficiency and low cytotoxicity. Besides, PAMA-PMEMA-PEG/siRRM2 also induced significant anti-tumor activity in vitro. These results indicated PAMA-PMEMA-PEG has potential for further use in the design of gene vehicles with the improved efficiency of siRNA delivery.

Azo-PROTAC: Novel Light-Controlled Small-Molecule Tool for Protein Knockdown.

Reversibly altering endogenous protein levels are persistent issues. Herein, we designed photoswitchable azobenzene-proteolysis targeting chimeras (Azo-PROTACs) by including azobenzene moieties between ligands for the E3 ligase and the protein of interest. Azo-PROTACs are light-controlled small-molecule tools for protein knockdown in cells. The light-induced configuration change can switch the active state to induce protein degradation activity, which can be reversely controlled by light exposure in intact cells. We compared the protein degradation abilities of Azo-PROTACs with different configurations and linker lengths. Using the stable form with the best degradation ability against the BCR-ABL fusion and ABL proteins in myelogenous leukemia K562 cells, we showed that Azo-PROTAC combines the potent protein knockdown and facile cell uptake properties of the small-molecule PROTAC with a reversible photoswitchability, offering a promising chemical knockdown strategy based on the light-induced reversible on/off properties.

HBXIP: a potential prognosis biomarker of colorectal cancer which promotes invasion and migration via epithelial-mesenchymal transition.

Hepatitis B X-interacting protein (HBXIP) is highly expressed in many cancers, but the correlation between the expression of HBXIP and the clinical significance and underlying molecular mechanisms in colorectal cancer (CRC) is still unclear. We selected 186 specimens from CRC patients for analyzing the relationship between the expression of HBXIP and the clinical-pathological features by immunohistochemistry. Migration and invasion experiments were performed to examine the effect of HBXIP on CRC cell metastasis. Besides, we also explored the possible molecular mechanism of HBXIP regulation of CRC cell metastasis by Western blot. Our data indicated that the HBXIP was overexpressed in CRC tissues. High HBXIP expression was correlated with metastasis and shorter survival times in patients with CRC and served as an independent factor for poor prognosis. Moreover, HBXIP promotes CRC metastasis by enhancing the epithelial-mesenchymal transition (EMT) process. Our findings provide the first evidence that HBXIP induces EMT to promote metastasis and predicts the poor prognosis of CRC. Therefore, HBXIP may become a new target for CRC treatment.

Metabolomics reveals the effect of valproic acid on MCF-7 and MDA-MB-231 cells.

1. Breast cancer is one of the most common malignancies in women worldwide. Metabolomics has been shown to be a promising strategy to elucidate the underlying pathogenesis of cancer and identify new targets for cancer diagnosis and therapy. Valproic acid (VPA), a histone deacetylase inhibitor, is a potential new drug in tumor therapy. This work used metabolomics to examine the effect of VPA on metabolism in breast cancer cells.2. Based on UPLC-MS/MS, we identified 3137 differential metabolites in human breast cancer MCF-7 cells and 2472 differential metabolites in human breast cancer MDA-MB-231 cells after VPA treatment.3. We selected 63 differential metabolites from MCF-7 samples and 61 differential metabolites from MDA-MB-231 cells with the more conspicuous changing trend. Furfural was up-regulated after VPA treatment in both cell lines. In both samples, VPA exerted an effect on the beta-alanine metabolism pathway and the taurine and hypotaurine metabolism pathway.4. This study identified the effect of VPA on metabolites and metabolic pathways in breast cancer cells, and these findings may contribute to the identification of new targets for breast cancer treatment.

Automatic Identification of Breast Ultrasound Image Based on Supervised Block-Based Region Segmentation Algorithm and Features Combination Migration Deep Learning Model.

Breast cancer is a high-incidence type of cancer for women. Early diagnosis plays a crucial role in the successful treatment of the disease and the effective reduction of deaths. In this paper, deep learning technology combined with ultrasound imaging diagnosis was used to identify and determine whether the tumors were benign or malignant. First, the tumor regions were segmented from the breast ultrasound (BUS) images using the supervised block-based region segmentation algorithm. Then, a VGG-19 network pretrained on the ImageNet dataset was applied to the segmented BUS images to predict whether the breast tumor was benign or malignant. The benchmark data for bio-validation were obtained from 141 patients with 199 breast tumors, including 69 cases of malignancy and 130 cases of benign tumors. The experiment showed that the accuracy of the supervised block-based region segmentation algorithm was almost the same as that of manual segmentation; therefore, it can replace manual work. The diagnostic effect of the combination feature model established based on the depth feature of the B-mode ultrasonic imaging and strain elastography was better than that of the model established based on these two images alone. The correct recognition rate was 92.95%, and the AUC was 0.98 for the combination feature model.

HPD overexpression predicts poor prognosis in breast cancer.

BACKGROUND: The enzyme, 4-hydroxyphenylpyruvate dioxygenase (HPD), is critical to tyrosine metabolism; its deficiency can cause tyrosinemia. However, its precise contribution to tumorigenesis is unclear. Here, we investigated the correlation between HPD expression and prognosis in patients with breast cancer. METHODS: 145 breast cancer specimens were selected to analyze HPD protein expression by immunohistochemistry and evaluate its relationship to patients' clinicopathological features. HPD localization was confirmed in MCF-7 and MDA-MB-231 breast cancer cells, using immunofluorescence staining. The expression of HPD protein was detected in breast cancer and cancer-adjacent normal tissues using Western blot analysis. Survival rates were calculated by the Kaplan-Meier method. RESULTS: We found that HPD protein was mainly located in the cytoplasm/nucleoli/perinucleus in breast cancer cells, as shown by immunofluorescence staining in MCF-7 and MDA-MB-231 cells, and immunohistochemistry in breast cancer and adjacent normal tissues (HPD protein expression-breast cancer: 46.9% [68/145], ductal carcinoma in situ [DCIS]: 22.6% [12/53], and normal tissues: only 4.8% [2/42]). Similarly, the Western blot results further confirmed the increased expression of HPD in breast cancer compared with cancer-adjacent normal tissues (P < 0.05). HPD expression level was positively correlated with histological grade and clinical stage, and inversely correlated with 10-year overall survival (OS) rates, in patients with breast cancer. Among patients with breast cancer, those with high HPD expression had worse OS rates than those with low HPD expression. Additionally, when patients were subgrouped by disease stage or grade, those with high HPD expression had worse OS rates than those with low HPD expression for each respective stage or grade. CONCLUSIONS: Our findings indicate that HPD may be a useful prognostic predictor, and a potential therapeutic target for patients with breast cancer.

Pectic polysaccharides extracted from Rauvolfia verticillata (Lour.) Baill. var. hainanensis Tsiang ameliorate ulcerative colitis via regulating the MAPKs and NF-κB pathways in dendritic cells.

This study was to investigate the effects and mechanisms of pectic polysaccharides (PP) extracted from Rauvolfia verticillata (Lour.) Baill. var. hainanensis Tsiang on dextran sulphate sodium (DSS)-induced ulcerative colitis (UC). Eighty female BALB/c mice were randomly divided into four groups: Control, DSS, DSS + salicylazosulfapyridine (SASP), and DSS+ PP. The disease activity index (DAI), overall physical activity, and blood stool were monitored daily to evaluate severity of UC. Histological scores of the colon were observed. The expression of nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPKs) pathways in colon tissues and bone marrow-derived dendritic cells (DCs) was assessed by western blot, immunohistochemistry, electrophoretic mobility shift assay (EMSA) and real time polymerase chain reaction (RT-PCR). Cytokines were measured by enzyme-linked immunosorbent assay (ELISA). The overall physical activity, DAI and histological scores decreased in DSS+SASP and DSS+PP groups, compared with the DSS-alone group. Also, tumour necrosis factor α (TNF-α) and interleukin 6 (IL-6) reduced significantly while the expression of IκBα was up-regulated, extracellular signal-regulated kinase (ERK), Jun N-terminal kinase (JNK) and p38 were activated, in DSS+SASP and DSS+PP groups. PP inhibited activation of MAPKs and NF-κB pathways in the bone-marrow-derived DCs. In conclusion, PP significantly ameliorated murine DSS-induced UC model, via regulation of MAPKs and NF-κB pathways in DCs.