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Nowadays customers would make decisions by reading online reviews and comparing differences in restaurants before visiting. Therefore how restaurants take advantage from such information is important to attract customers and stay competitive. Many researchers believe that increasing business performance could improve competitiveness. However, with changing customer requirements and business environment, it is challenging to understand which attributes matter the most to customers and how to improve considering competitors. Therefore this study proposed assessing restaurant competitiveness using online reviews. After crawling 38,479 online reviews employing Python, deep learning-based BERT is developed to measure attribute performance and understand the competitiveness through McKinsey Matrix. Then, the competitiveness was analyzed from a temporal dynamic view to present how attributes are changing importance. Notably, the asymmetric effects between attribute performance and satisfaction were considered. Results demonstrated encouraging accuracy in measuring restaurant competitiveness and explained how asymmetric McKinsey Matrix could help formulate efficient competitiveness enhancement strategies. • Develops a deep learning-based BERT to accurately assess restaurant competitiveness. • Incorporates asymmetric effects to formulate competitiveness enhancement strategies. • Considers how attributes are changing competition position over temporal dynamics. • Improves McKinsey Matrix for efficient restaurant competitiveness analysis. [ABSTRACT FROM AUTHOR]

Wilderness is of great value and conservation significance. An in-depth understanding of the evolution of the spatial distribution of wilderness conditions in China and the factors influencing them is crucial for biodiversity conservation and restoration. However, the evolution of its spatial and temporal patterns and the factors influencing them have been little explored in studies of wilderness. In this study, the Weighted Linear Combination model was utilized to assess the quality of wilderness in China over the past 20 years, and the geographic detector model assessed the key factors that have influenced wilderness. The study results indicate that (1) Over the past 20 years, the western wilderness has worsened, while the eastern and central regions have seen some improvement. (2) Changes in wilderness quality are mainly influenced by the temperature and the distribution of nature reserves. (3) High wilderness quality areas are mainly influenced by actual evapotranspiration and temperature, while population density and GDP play a dominant role in most medium and low wilderness quality areas. (4) Interacting factors are greater than any single factor affecting wilderness. The results of the study can provide a reference for the conservation and management of wilderness resources and biodiversity in China. [Display omitted] • Wilderness quality improved in >60% of Chinese provinces, but declined in Xizang (45.3%) and Xinjiang (50.8%). • Changes in wilderness quality are mainly influenced by the temperature and nature reserves distribution. • The dominant factors affecting wilderness quality differ depending on the region. [ABSTRACT FROM AUTHOR]

We analyse the impact of the collapse of Silicon Valley Bank (SVB) on the causal structure using a sequence of high-frequency transfer entropy networks. Calculations show that the event significantly affected the causal structure of the banking sector and that companies with high market capitalisation had stronger influence after the event. Finally, path-based indicators suggest that SVB had significant influence before the crisis. • This study used high-frequency data to analyse the impact of the collapse of Silicon Valley Bank (SVB). • This study analysed the causal structure of extreme values using networks and transfer entropy. • SVB did not have a strong direct impact on the banking sector before its collapse. • The collapse of SVB has significantly affected the structure of information flows in the banking sector. • High-capitalisation companies have a stronger impact after March 9th. [ABSTRACT FROM AUTHOR]

Di-(2-ethylhexyl) phthalate (DEHP) is a widely used plasticizer known for its environmental endocrine-disrupting properties, posing potential risks to various organs. However, the precise impact of DEHP on intestinal health and its contribution to the initiation of intestinal inflammation remains elucidated. This study aims to investigate the underlying mechanisms of DEHP-induced intestinal inflammation in mice, specifically focusing on the complex interplay between the gut microbiota-metabolite axis and associated pathophysiological alterations. Our findings showed that DEHP-induced damage of multiple organs systemically, as indicated by abnormal liver and kidney biochemical markers, along with a disrupted ileum morphology. Additionally, DEHP exposure disrupted gut barrier function, causing intestinal inflammation characterized by bacterial translocation and alterations in defense and inflammation-related gene expressions. Moreover, 16S rRNA analysis suggested that DEHP-induced gut microbial remodeling is characterized by an upregulation of detrimental bacteria (Erysipelotrichaceae) and a downregulation of beneficial bacteria (Muribaculaceae, Ruminococcaceae, and Lachnospiraceae). Metabolomics analysis revealed DEHP perturbed gut metabolic homeostasis, particularly affecting the degradation of aromatic compounds, which generated an aberrant activation of the AhR and NF-κB, subsequently causing intestinal inflammation. Consequently, our results elucidate the mechanistic link between disrupted gut microbiota and metabolome and the initiation of DEHP-induced intestinal inflammation, mediated through the AhR/NF-κB signaling pathway. [Display omitted] • DEHP induces systemic multiple organ damage in mice. • DEHP causes the imbalance of intestinal homeostasis and bacterial migration. • DEHP induces the imbalance of gut microbiota homeostasis and the change of metabolites. • DEHP induces intestinal inflammation by activating the AhR/NF-κB pathway. [ABSTRACT FROM AUTHOR]

Atrazine (ATR), a water-soluble herbicide commonly used to control broad-leaf and monocotyledonous weeds, presents a significant risk to environmental soil and water quality. Exposure to ATR adversely affects human and animal health, frequently resulting in cardiac impairment. Curcumin (Cur), an acidic polyphenol derivative from plants acclaimed for its pronounced anti-inflammatory and antioxidant properties, has garnered interest as a potential therapeutic agent. However, whether it has the potential to ameliorate ATR-induced cardiac toxicity via modulation of endoplasmic reticulum stress (ERS) and apoptosis pathways in mice remains unclear. Our results showed that Cur supplementation attenuates ATR-induced cardiotoxicity, evidenced by decrease in creatine kinase and lactate dehydrogenase, key biochemical markers of myocardial injury, which have a more significant protecting effect in high-dose ATR induced injury. Histopathological and electron microscopy examinations further solidified these findings, demonstrating an amelioration in organellar damage, particularly in endoplasmic reticulum swelling and subsequent mitochondrial impairment. Additionally, ATR exposure augments ERS and triggers apoptotic pathways, as indicated by the upregulation of ERS-related gene expression (ATF6, CHOP, IRE1, GRP78) and pro-apoptotic markers (BAX, BAK1, Caspase3, Caspase. Intriguingly, Cur counteracts this detrimental response, significantly reducing ERS and pro-apoptotic signals at both transcriptional and translational levels. Collectively, our findings illuminate Cur's cardioprotective effect against ATR-induced injury, primarily through its anti-ERS and anti-apoptotic activities, underscoring Cur's potential as a therapeutic for ATR-induced cardiotoxicity. [ABSTRACT FROM AUTHOR]

Including members of the public in the development of effective environmental monitoring systems is gaining traction. This research assesses the potential for a hybrid monitoring system for the case of coral at the Great Barrier Reef. Based on a review of citizen-derived data sources, the paper first develops a framework and then populates it with five datasets. These are then compared based on data volumes, type of data, spatial coverage, and bleaching patterns. The results reveal the inherent difficulties – both in terms of quantity and quality – for collective sensing data (Twitter in this case) and more structured human sensors approaches (Eye on the Reef Sightings). However, more targeted approaches, such as CoralWatch and tourism-operator based data collection, emerged as important contributors to information generation on the state of coral. Citizen-based data that either deliver a high data density per location, a wide geographic coverage, or regular observations over time are particularly valuable. Recommendations are made for developing a hybrid monitoring system that integrates citizen-derived with professionally collected data. • Framework for differentiating various approaches to citizen-derived data • Comparison of five data sources for coral at the Great Barrier Reef • Collective sensing data are insufficient in quantity and quality. • Structured citizen science programs can add considerable value. • A hybrid monitoring system could greatly assist the marine park authority. [ABSTRACT FROM AUTHOR]

In the dynamic field of destination management, maintaining a destination's competitiveness requires understanding the evolving preferences of tourists. However, current research often adopts a static approach, failing to capture the dynamic nature of tourist needs and the evolving competitiveness of a destination. To address this, we introduce a novel approach using user-generated content from various social media platforms over a six-year period to assess key attributes that influence destination competitiveness. The results indicate that attributes in deciding destination competitiveness are not fixed, with some remaining stable factors in competitiveness, while others fluctuate over time. Attributes that even alter their competitive standing could significantly impact overall destination competitiveness. This research contributes a dynamic model that allows destination managers to adapt strategies in real time, aligning with current market conditions and enhancing competitiveness in the tourism industry. [ABSTRACT FROM AUTHOR]

Background: Colorectal cancer is associated with ulcerative colitis (UC). The infiltration of neutrophils is the main cause of DNA damage produced by inflammation in the intestinal epithelium. Under the action of peptidyl arginine deaminase 4 (PAD4), neutrophils dissociate chromatin and form neutrophil extracellular traps (NETs), which can aggravate tissue inflammation and encourage tumor development. Although Huang Qin Decoction (HQD) was found to be useful in treating UC and was used to gradually prevent and treat digestive tract cancers, the underlying reasons were unclear.Methods: To demonstrate HQD could inhibits the initiation of colitis associated carcinogenesis by controlling NETs related inflammation, we first performed an AOM/DSS-generated colitis-associated carcinogenesis model to assess the efficacy of HQD in reducing neutrophil infiltration and anti-tumor activity. Then, using network pharmacology research, we investigated the potential mechanisms underlying those medicinal effects, as demonstrated by the detection of NETs aggregation and PAD4 expression changes in the colon.Results: HQD substantially reduced the number of colon cancers and the expression of Ki67, restored the level of intestinal tight junction protein occludin and ZO-1, and relieved the intestinal inflammation caused by TNF-α, IL-1β. At the same time, it inhibited neutrophil infiltration in the colon and improved the immunosurveillance of CD8+T cells. The potential mechanisms of HQD intervention against UC and UC with neoplasia (UCN) were studied using network pharmacology, and 156 conjunct genes as well as numerous inflammation-related pathways were identified. Protein-protein interaction (PPI) analysis indicated that HQD inhibition of intestinal tumors might be related to the deactivation of PAD4, which was verified by the down-regulation of NETs, MPO-DNA complex levels, and PAD4 expression after HQD treatment.Conclusion: Huang Qin Decoction inhibits the initiation of colitis associated carcinogenesis by controlling PAD4-dependent neutrophil extracellular traps. [ABSTRACT FROM AUTHOR]

This paper introduces an innovative approach for assessing visitor satisfaction at the destination level by identifying attributes of interest from social media text and indirectly measuring performance and importance values. A lexicon-based method for sentiment analysis is applied to determine performance value at the destination level, while importance is calculated using an adjusted association rule mining algorithm. The results are validated with earlier survey-based attributes relevant to visitors and Australia's case. The results demonstrate encouraging accuracy, suggesting that the proposed methodology offers opportunities to assess tourist satisfaction at destinations with larger sample sizes for a lower cost and greater data collection flexibility than traditional approaches. The methods proposed could be beneficial in a wide range of tourism contexts. • Destinations are recognized from tourists' travel itineraries. • Sentiment analysis is applied to identify performance at multiple destinations. • The importance of each attribute is calculated proportionally at each destination. • Validated results of social media data with survey data [ABSTRACT FROM AUTHOR]

Growing concern about the climate crisis comes with increased scrutiny of flying as an emission-intensive activity. This study conceptualises a modern communication system and draws on social media data to examine pre-COVID-19 (September to December 2019) public conversations about aviation and climate change. The analysis of >326,000 Twitter posts reveals that issue salience can be considerable at times, especially during key events such as United Nation climate summits and for users from countries such as Portugal, Puerto Rico, Qatar, France and Spain. Topic modelling identified five key frames: economy and industry, public opinion, fairness and conflict, consequences and responsibility. The fairness and conflict frame recorded the largest number of tweets, and was noteworthy for its negative sentiment. It also had the highest retweet rate and the densest network in terms of average users per community. The responsibility frame was interesting for its positive sentiment, and perhaps the opportunity for aviation stakeholders to contribute proactively to the conversations by sharing climate action success stories. Given the importance of public opinion (voters and consumers), and the link between media activity and policy decisions, the ongoing monitoring of issue salience, frames and peer groups related to flying and climate change seems beneficial. • Machine learning approach to monitoring social media discussions on aviation and climate change. •Aviation is a salient topic within climate change discussions on Twitter. •There are pronounced peaks in salience, often in association with key events. •Five frames have been identified from the aviation climate change social media activity. •The fairness and conflict frame is most prominent and negative and requires stakeholder attention. [ABSTRACT FROM AUTHOR]

• A novel and innovative way of tracking Chinese visitors' mobility to Australia and other world regions • Mining data from Chinese social media Sina Weibo to understand their travel pattern • Hight resolution of data visualisation • Discover new dimension of global mobility [ABSTRACT FROM AUTHOR]

Abstract: Single-crystalline SnO2 nanorods with large aspect ratios have been synthesized in poly (ethylene glycol) 200 (PEG-200) medium. The products are characterized by X-ray diffraction (XRD), transmission electron microscopy (TEM) and high resolution transmission electron microscopy (HRTEM). The results indicate that the average diameter and length of the nanorods are 13nm and 550nm, respectively, presenting a mean aspect ratio of 42. These SnO2 nanorods show typical rutile phase and exhibit preferential growth along the [] direction. A proposed mechanism for the formation of SnO2 nanorods has also been discussed. In addition, photocatalytic activity study indicates that the as-prepared SnO2 nanorods present excellent photocatalytic degradation of Rhodamine B (RhB). When irradiated by a 300W high-pressure mercury lamp, the degradation of RhB reaches 100% within 45min. [Copyright &y& Elsevier]

Background: Intestinal epithelial barrier dysfunction, which involves myosin light chain kinase (MLCK) activation, contributes to the occurrence and progression of inflammation in inflammatory bowel disease (IBD). Wogonoside helps maintain intestinal homeostasis in mice with dextran sulfate sodium (DSS)-induced colitis, but it is unclear whether it modulates intestinal barrier function.Purpose: Here, we demonstrate that wogonoside protects against intestinal barrier dysfunction in colitis via the MLCK/pMLC2 pathway both in vivo and in vitro.Methods: Caco-2 cell monolayers treated with the proinflammatory cytokine TNF-α showed barrier dysfunction and were assessed in the absence and presence of wogonoside for various physiological, morphological, and biochemical parameters. Colitis was induced by 3% DSS in mice, which were used as an animal model to explore the pharmacodynamics of wogonoside. We detected MLCK/pMLC2 pathway proteins via western blot analysis, assessed the cytokines IL-13 and IFN-γ via ELISA, tested bacterial translocation via fluorescence in situ hybridization (FISH) and a proper sampling of secondary lymphoid organs for bacterial culture. In addition, the docking affinity of wogonoside and MLCK was observed with DS2.5 software.Results: Wogonoside alleviated the disruption of transepithelial electrical resistance (TER) in TNF-α exposured Caco-2 cell; FITC-dextran hyperpermeability; loss of the tight junction (TJ) proteins occludin, ZO-1 and claudin-1 in Caco-2 cell monolayers; and bacterial translocation in colitic mice. Moreover, wogonoside reduced the levels of the proinflammatory cytokines IL-13 and IFN-γ to maintain intestinal immune homeostasis. Transmission electron microscopy (TEM) confirmed that wogonoside ameliorated the destruction of intestinal epithelial TJs. Wogonoside not only inhibited the cytoskeletal F-actin rearrangement induced by TNF-α, stabilized the cytoskeletal structure, suppressed MLCK protein expression, and reduced MLC2 phosphorylation. In addition, the results of molecular docking analysis showed that wogonoside had a high affinity for MLCK and formed hydrogen bonds with the amino acid residue LYS261 and π bonds with LYS229.Conclusion: Collectively, our study indicates that wogonoside alleviates colitis by protecting against intestinal barrier dysfunction, and the potential mechanism may involve regulation of TJs via the MLCK/pMLC2 signaling pathway. Meanwhile, our study also explains the success of S. baicalensis in the treatment of ulcerative colitis (UC). [ABSTRACT FROM AUTHOR]

Fatty liver hemorrhagic syndrome (FLHS) is a prevalent metabolic disorder observed in egg-laying hens, characterized by fatty deposits and cellular steatosis in the liver. Our preliminary investigations have revealed a marked decrease in the concentration of butyric acid in the FLHS strain of laying hens. It has been established that sodium butyrate (NaB) protects against metabolic disorders. However, the underlying mechanism by which butyrate modulates hepato-lipid metabolism to a great extent remains unexplored. In this study, we constructed an isolated in vitro model of chicken primary hepatocytes to induce hepatic steatosis by free fatty acids (FFA). Our results demonstrate that treatment with NaB effectively mitigated FFA-induced hepatic steatosis in chicken hepatocytes by inhibiting lipid accumulation, downregulating the mRNA expression of lipo-synthesis-related genes (sterol regulatory element binding transcription factor 1 ( SREBF1 ), acetyl-CoA carboxylase 1( ACC1 ), fatty acid synthase ( FASN ), stearoyl-CoA desaturase 1 ( SCD1 ), liver X receptor α ( LXRα ), 3-hydroxy-3-methylglutaryl-CoA reductase ( HMGR )) (P < 0.05), and upregulating the mRNA and protein expression of AMP-activated protein kinase α1 (AMPKα1), peroxisome proliferator-activated receptor α (PPARα), and carnitine palmitoyl-transferase 1A (CPT1A) (P < 0.05). Moreover, AMPK and PPARα inhibitors (Compound C (Comp C) and GW6471, respectively) reversed the protective effects of NaB against FFA-induced hepatic steatosis by blocking the AMPK/PPARα pathway, leading to lipid droplet accumulation and triglyceride (TG) contents in chicken primary hepatocytes. With these findings, NaB can alleviate hepatocyte lipoatrophy injury by activating the AMPK/PPARα pathway, promoting fatty acid oxidation, and reducing lipid synthesis in chicken hepatocytes, potentially being able to provide new ideas for the treatment of FLHS. [ABSTRACT FROM AUTHOR]

Triclosan (TCS) is an antimicrobial compound incorporated into more than 2000 consumer products. This compound is frequently detected in the human body and causes ubiquitous contamination in the environment, thereby raising concerns about its impact on human health and environmental pollution. Here, we demonstrated that 20 weeks' exposure of TCS drove the development of glucose intolerance by inducing compositional and functional alterations in intestinal microbiota in rats. Fecal-transplantation experiments corroborated the involvement of gut microbiota in TCS-induced glucose-tolerance impairment. 16S rRNA gene-sequencing analysis of cecal contents showed that TCS disrupted the gut microbiota composition in rats and increased the ratio of Firmicutes to Bacteroidetes. Cecal metabolomic analyses detected that TCS altered host metabolic pathways that are linked to host glucose and amino acid metabolism, particularly branched-chain amino acid (BCAA) biosynthesis. BCAA measurement confirmed the increase in serum BCAAs in rats exposed to TCS. Western blot and immunostaining results further confirmed that elevated BCAAs stimulated mTOR, a nutrient-sensing complex, and following IRS-1 serine phosphorylation, resulted in insulin resistance and glucose intolerance. These results suggested that TCS may induce glucose metabolism imbalance by regulating BCAA concentration by remodeling the gut microbiota. • Chronic triclosan exposure results in impaired glucose tolerance in rats. • Triclosan exposure induced the gut-microbe composition variation. • Branched-chain amino acids metabolism was affected by triclosan exposure. [ABSTRACT FROM AUTHOR]

RANKL induces osteoclastogenesis via JNK1 signal that exerts an anti-apoptotic effect during osteoclastogenesis. However, the classic downstream c-Jun/AP-1 pathway is not included in anti-apoptosis of JNK1. Thus, the detail mechanism underlying JNK1-resisted apoptosis remains unknown during RANKL-induced osteoclastogenesis. RANKL-induced autophagy results in the degradation of the osteoclastogenesis-inhibitor TRAF3, and TRAF3 is thought as a regulator of apoptosis. Given the key effect of JNK1 in mediating autophagy, our study aims to investigate the significance of TRAF3 in bridging JNK1-mediated autophagy and apoptotic resistance during osteoclastogenesis. In this study, by using Bone Marrow-derived macrophages (BMMs) as osteoclast precursors (OCPs), we found that RANKL-induced TRAF3 degradation was significantly suppressed by JNK inhibitor (SP600125), which was restored by overexpression of Beclin1 (key autophagic protein). Nevertheless, TRAF3 silencing partially reversed the reduced osteoclastogenesis under SP600125 intervention. Besides, OCP apoptosis was positively regulated by TRAF3 overexpression, regardless of the application of autophagy inhibitor or SP600125. Remarkably, the enhanced apoptosis caused by the pharmacological inhibition of Beclin1 was reversed by TRAF3 silencing. Together, these results suggest that JNK1-mediated autophagy could promote RANKL-induced osteoclastogenesis via enhancing TRAF3 degradation. Importantly, JNK1 could prevent OCP apoptosis through autophagy-TRAF3 signaling, which provides more potential targets for clinical treatment of pathological bone loss. • TRAF3 silencing reversed the reduced osteoclastogenesis by JNK1 inhibitior. (74). • TRAF3 could bridge autophagy and apoptosis in OCPs. (50). • JNK1-autophagy-TRAF3-apoptosis pathway is independent of classical c-Jun/AP-1 pathway. (85). [ABSTRACT FROM AUTHOR]

Abstract Ethnopharmacology relevance Rhubarb Peony Decoction (RPD) is a formula of traditional Chinese medicine chronicled in Jin Gui Yao Lve , commonly used to treat ulcerative colitis (UC). However, the underlying mechanism of RPD treating UC remains elusive. In our study, we investigated the therapeutic efficacy of RPD and potential mechanism involved in inhibiting dextran sulfate sodium (DSS)-induced ulcerative colitis in mice. Methods The colitis was induced by DSS in mice for 5 days and estimated body weight loss, disease activity index (DAI) and colon length. Histological changes were observed by H&E staining. The number and abundance of gut mircrobiota were measured with 16 S rDNA sequencing. GC-MS was used to detect the concentration of short chain fatty acids (SCFAs) in cecum. Flow cytometry analyzed the proportion of Th17 and Treg cells in mesenteric lymph nodes (MLNs). IL-17A and Foxp3 in colon were determined by immunohistochemical analyses. The level of cytokine was determined by Multi-Analyte Flow Assay Kit. Results Administration of RPD significantly alleviated the pathological changes of UC mice, involving rescued the inflammation-related reduction of colon length, ameliorated body weight loss and damaged tissue. In addition, RPD altered the gut microbiota, involving restored α diversity, increased significantly the abundance of Firmicutes and Actinobacteria, decreased the Proteobacteria and Bacteroidetes. Furthermore, the number of Butyricicoccus pullicaecorum, a butyrate-producing bacterium, were augmented obviously by RPD. Besides, RPD restored the content of SCFA in intestinal tract. Additionally, the proportion of Th17 cells and Treg cells in mesenteric lymph nodes, likewise, the expression of IL-17A and Foxp3 in colon were regulated by RPD, contributing to the restoration of Th17/Treg balance. Moreover, RPD significantly decreased the level of IL-6, TNF-α, IFNγ, IL-10, IL-17A, IL-21, IL-22 in colon, simultaneously increased Treg-related cytokine TGF-β at dose-dependently. Conclusions These results demonstrated that RPD had effect on ulcerative colitis, which was related to regulating gut microbiota, especially Butyricicoccus pullicaecorum, and SCFAs to restore the gut Th17/Treg homeostasis. Graphical abstract fx1 [ABSTRACT FROM AUTHOR]

Gestational diabetes mellitus (GDM), which has an increasing global prevalence, contributes to the susceptibility to metabolic dysregulation and obesity in the offspring via epigenetic modifications. However, the underlying mechanism remains largely obscure. The current study established a GDM mice model to investigate the alternations in the metabolic phenotypes and genomic DNA methylation in the pancreas of the offspring. We found that in the GDM offspring, intrauterine hyperglycemia induced dyslipidemia, insulin resistance, and glucose intolerance. Meanwhile, altered DNA methylation patterns were exhibited in the pancreas and many differentially methylated regions (DMRs)-related genes were involved in glycolipids metabolism and related signaling pathways, including Agap2, Plcbr, Hnf1b, Gnas, Fbp2, Cdh13, Wnt2, Kcnq1, Lhcgr, Irx3, etc. Additionally, the overall hypermethylation of Agap2, verified by bisulfite sequencing PCR (BSP), was negatively correlated with its mRNA expression level. In conclusion, these findings suggest that the DNA methylation changes in the pancreatic genome of the GDM offspring may be associated with the glycolipid metabolism abnormalities, T2DM susceptibility, and obesity in the adult GDM offspring. [ABSTRACT FROM AUTHOR]

Background The prevalence of allergic rhinitis has risen sharply. Previous work has demonstrated the anti-inflammatory effect of catechin, including in models of allergic disease. However, the molecular mechanisms underlying this therapeutic effect remain unclear. Thymic stromal lymphopoietin(TSLP), as a molecule from epithelial cell, has been identified that plays a significant role in the development of allergic disease, and the production of TSLP is related to activation of the NF-κB signaling pathway. For that, we try to research the treatment of catechin for allergic rhinitis and found out possible mechanism under this effect, which was based on TSLP factor. Materials and methods Here, the anti-inflammatory effects of catechin were studied in an ovalbumin-induced allergic rhinitis murine model and a vitro experiments using poly(I:C)-stimulated human nasal epithelial cells(HNEpCs). The pharmacological effects of catechin in allergic rhinitis mice were assessed by observing the allergic symptoms, performing hematoxylin and eosin staining and Giemsa staining of the nasal tissues. Additionally, the TSLP expression in epithelial cells was tested by enzyme-linked immunosorbent assays, immunohistochemistry, and western blots. The serum levels of interleukin-5, interleukin-13, and ovalbumin-specific immunoglobulin-E were detected by enzyme-linked immunosorbent assays, and the balance between T helper type 1 and T helper type 2 cells was assessed by flow cytometry. The expression levels of phospho-NF-κBp65, IκBα, and NF-κBp65 proteins were further investigated by western blots or immunofluorescence. Results Our results reveal that catechin, in doses of 75, 150, or 300 mg/kg, remitted the allergic symptoms in mice with allergic rhinitis, like sneezing and nasal rubbing. Catechin could reduce the levels of interleukin-5, interleukin-13, and ovalbumin-specific immunoglobulin-E in the serum and restored the T helper type 2/T helper type 1 cell balance and also had anti-thymic stromal lymphopoietin effects. Moreover, as an upstream regulator of TSLP, the NF-κB signal pathway was also suppressed after catechin treatment, which was demonstrated by the observed decrease in phospho-NF-κBp65 and NF-κBp65 levels and the reduction of IκBα degradation and NF-κBp65 nuclear translocation. Conclusions Catechin effectively reduced the inflammation in allergic rhinitis. The underlying mechanism is that catechin inhibited the expression of TSLP in epithelial cells by influencing NF-κB/TSLP pathway. [ABSTRACT FROM AUTHOR]