Oxymatrine alleviates NSAID-associated small bowel mucosal injury by regulating MIP-1/CCR1 signalling and gut microbiota.

Oxymatrine (OMT) as a quinazine alkaloid extracted from matrine has been shown to exhibit anti-inflammatory and anti-tumour effects. However, the protective mechanism of OMT on NSAID-associated small bowel mucosal injury remains unreported. We found that OMT could improve the clinical symptoms and pathological inflammation scoring, reduce the secretion of proinflammatory cytokines IL-1β, IL-6 and TNF-α and cell apoptosis, promote cell proliferation and protect intestinal mucosal barrier as compared with the Diclofenac Sodium (DS) group.

CircUGGT2 downregulation by METTL14-dependent mA modification suppresses gastric cancer progression and cisplatin resistance through interaction with miR-186-3p/MAP3K9 axis.

Chemoresistance is a major therapeutic challenge in advanced gastric cancer (GC). N-methyladenosine (mA) RNA modification has been shown to play fundamental roles in cancer progression. However, the underlying mechanisms by which mA modification of circRNAs contributes to GC and chemoresistance remain unknown.

Detachable string magnetically controlled capsule endoscopy for the noninvasive diagnosis of esophageal diseases: A prospective, blind clinical study.

Background: Traditional esophagogastroduodenoscopy (EGD), an invasive examination method, can cause discomfort and pain in patients. In contrast, magnetically controlled capsule endoscopy (MCE), a noninvasive method, is being applied for the detection of stomach and small intestinal diseases, but its application in treating esophageal diseases is not widespread.

Aim: To evaluate the safety and efficacy of detachable string MCE (ds-MCE) for the diagnosis of esophageal diseases.

mA reader YTHDF3 is associated with clinical prognosis, related RNA signatures and immunosuppression in gastric cancer.

Background: YTHDF3 as a N6-methyladenosine (m6A) reader participates in the development and progression of multiple cancer types, however, the prognosis, molecular biology and immune infiltration of YTHDF3 in gastric cancer (GC) have not been investigated.

Methods: The YTHDF3 expression profile and clinicopathological parameters of stomach adenocarcinoma (STAD) were downloaded from TCGA. The online websites and databases such as GEPIA2, cBioPortal, UALCAN, ImmuCellAl, xCell, TISIDB, GSCA were utilized for analysis of the association of YTHDF3 with STAD, including clinical prognosis, WGCNA and LASSO Cox regression analysis.

METTL16-mediated translation of promotes non-alcoholic fatty liver disease progression m6A-dependent manner.

Background: As the most prevalent chemical modifications on eukaryotic mRNAs, N6-methyladenosine (m6A) methylation was reported to participate in the regulation of various metabolic diseases. This study aimed to investigate the roles of m6A methylation and methyltransferase-like16 (METTL16) in non-alcoholic fatty liver disease (NAFLD).

Methods: In this study, we used a model of diet-induced NAFLD, maintaining six male C57BL/6J mice on high-fat diet (HFD) to generate hepatic steatosis.

Alterations in the saliva microbiome in patients with gastritis and small bowel inflammation.

The oral microbiome is an important part of the human microbiome. Accumulating data have shown that oral microbiome alterations are closely related to multiple human diseases. However, salivary microbiota distributions remain unclear in patients with gastritis and small bowel inflammation.

METTL14-mediated mA modification of circORC5 suppresses gastric cancer progression by regulating miR-30c-2-3p/AKT1S1 axis.

Background: N6-methyladenosine (mA) RNA methylation and circular RNAs (circRNAs) have been shown to act vital roles in multiple malignancies including gastric cancer (GC). However, there is little knowledge about how mA modification of circRNAs contributes to GC progression.

Methods: The association of METTL14 expression with the clinicopathological characteristics and prognosis in patients with GC was assessed by Western blot, Immunohistochemistry and public datasets.

Dihydroartemisinin Suppresses the Tumorigenesis and Cycle Progression of Colorectal Cancer by Targeting CDK1/CCNB1/PLK1 Signaling.

Dihydroartemisinin (DHA), a well-known antimalarial drug, has been widely investigated for its antitumor effects in multiple malignancies. However, its effects and regulatory mechanisms in colorectal cancer (CRC) are still unproved. In this study, experiments including CCK8, EdU, Transwell, and flow cytometry analyses and an tumorigenesis model were conducted to assess the effects of DHA on the bio-behaviors of CRC cells.

CircPTK2 inhibits the tumorigenesis and metastasis of gastric cancer by sponging miR-134-5p and activating CELF2/PTEN signaling.

Background: CircRNAs are a new subset of noncoding RNAs formed by covalent closed loops and play crucial roles in the regulation of cancer gene expression. However, the roles and underlying mechanisms of circRNAs in gastric cancer (GC) remain indistinct. This study aimed to explore the role and mechanism of hsa_circ_0006421 (circPTK2) in GC.

The Detective Value of Magnetically Controlled Robotic Capsule Endoscopy in Patients With Suspected Small Intestinal Disease.

To explore the detective value of magnetically controlled robotic capsule endoscopy (MCRCE) in patients with suspected small intestinal disease. In total, 1,802 patients with suspected small intestinal disease and negative gastroenteroscopy from Shanghai Jiao Tong University Affiliated Sixth People's Hospital were examined with MCRCE, and the data were collected for further analysis. Among the 1,802 patients who were examined with MCRCE, 974 were diagnosed with small intestinal disease, reaching a positive detection rate of 54.

The mA Reader YTHDF1 Facilitates the Tumorigenesis and Metastasis of Gastric Cancer via USP14 Translation in an mA-Dependent Manner.

Objectives: N-methyladenosine (mA) RNA methylation is implicated in the progression of multiple cancers via influencing mRNA modification. YTHDF1 can act as an oncogene in gastric cancer (GC), while the biological mechanisms via which YTHDF1 regulates gastric tumorigenesis through mA modification remain largely unknown.

Methods: GEO and TCGA cohorts were analyzed for differentially expressed mA modification components in GC clinical specimens and their association with clinical prognosis.

Mucosal microbiome dysbiosis associated with duodenum bulb inflammation.

Background: There is high morbidity in clinical patients with duodenum bulb inflammation. Mucosa-associated microbiota, which are closely related to inflammatory processes, may have a pathogenic role, but the duodenum bulb microbial signature is poorly studied.

Objective: This study aimed to characterize microbial changes associated with duodenum bulb inflammation.

Dihydroartemisinin inhibits the tumorigenesis and invasion of gastric cancer by regulating STAT1/KDR/MMP9 and P53/BCL2L1/CASP3/7 pathways.

Dihydroartemisinin (DHA), an effective antimalarial drug, has been widely investigated as an anti-tumor agent. Although previous studies have indicated the potential therapeutic effects of DHA on multiple malignancies, its detailed molecular mechanisms in gastric cancer (GC) are still undocumented. In the present study, we applied network pharmacology and bioinformatics (gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses) to obtain the collective targets of DHA and GC and analyzed their involvement in constructing a protein-protein interaction (PPI) network.

Dihydroartemisinin prevents dextran sodium sulphate-induced colitisthrough inhibition of the activation of NLRP3 inflammasome and p38 MAPK signaling.

Dihydroartemisinin (DHA), a sesquiterpene lactone derived from artemisinin, has been reported to possess anti-inflammation and anti-cancer activities. But its underlying protective mechanisms on dextran sodium sulphate (DSS)-induced colitis remain rarely reported. We applied a network pharmacology approach to predict the collective targets of DHA and acute colitis.

Network pharmacology-based identification of the antitumor effects of taraxasterol in gastric cancer.

Taraxasterol (TAX), a pentacyclic triterpene, has been reported to exhibit potent antitumor activity. However, the effects and molecular mechanisms of TAX in gastric cancer (GC) remain undocumented. A network pharmacology approach was applied to identify the collective targets of TAX and GC.

Rewiring of Microbiota Networks in Erosive Inflammation of the Stomach and Small Bowel.

The development of non-invasive, inexpensive, and effective early diagnosis tests for gastric and small-bowel lesions is an urgent requirement. The introduction of magnetically guided capsule endoscopy (MGCE) has aided examination of the small bowel for diagnoses. However, the distribution of the fecal microbiome in abnormal erosions of the stomach and small bowel remains unclear.

Mild changes in the mucosal microbiome during terminal ileum inflammation.

Patients with inflammation in the terminal ileum have high morbidity. In genetically susceptible hosts, chronic intestinal inflammation targeting the resident intestinal microbiota develops, but the microbial signature of the terminal ileum is poorly studied. To improve understanding of the mechanisms underlying the high prevalence of terminal ileum inflammation, we used 16S rRNA sequencing to analyse the mucosa-associated microbiota of the terminal ileum under intestinal homeostasis and inflammation conditions.

Dihydroartemisinin inhibits the growth and invasion of gastric cancer cells by regulating cyclin D1-CDK4-Rb signaling.

Background: Dihydroartemisinin (DHA), a semisynthetic derivative of artemisinin, has a broad range of biological properties, including antitumor activity. However, the mechanisms by which DHA affects the tumorigenesis of gastric carcinoma (GC) are poorly understood.

Material And Methods: The targets of DHA were identified by network pharmacology, and the association of CDK4 with clinicopathological characteristics and prognosis in patients with GC was analyzed by using TCGA data.

The long non-coding RNA promotes gastric cancer by activating the phosphatidylinositol 3-kinase/AKT pathway.

Long non-coding RNAs contribute to the development of human cancers. We compared the long non-coding RNA levels in gastric cancer (GC) and para-cancerous tissues in the Gene Expression Omnibus, and found that small nucleolar RNA host gene 12 () was upregulated in GC tissues. Fluorescence in situ hybridization confirmed that is overexpressed in GC tissues.

Macrophages-derived p38α promotes the experimental severe acute pancreatitis by regulating inflammation and autophagy.

Background: Severe acute pancreatitis (SAP) is a common threat to human health. In the present study, we aimed to investigate the underlying mechanisms by which p38α in macrophages contributes to SAP. We used conditional knockout of p38α in macrophages and p38 MAPK inhibitors to understand the effects of p38α in macrophages on caerulein-induced inflammatory responses in SAP mice models.

Sanguinarine inhibits the tumorigenesis of gastric cancer by regulating the TOX/DNA-PKcs/ KU70/80 pathway.

Sanguinarine (SAG), a benzophenanthridine alkaloid extracted from Sanguinaria canadensis, exerts antioxidant, anti-inflammatory and antiproliferative activities in a variety of malignancies. However, the underlying mechanisms by which SAG affects the tumorigenesis of gastric cancer (GC) are unclear. The common targets of SAG and GC were identified by network pharmacology, and the association of thymocyte selection-associated high mobility group box (TOX) with the clinicopathological characteristics and prognosis of patients with GC was analyzed by using datasets from The Cancer Genome Atlas (TCGA).

Taraxacum officinale extract ameliorates dextran sodium sulphate-induced colitis by regulating fatty acid degradation and microbial dysbiosis.

Numerous data show that taraxacum officinale extract (TOE) exerts protective effects on inflammatory diseases. However, the underlying mechanisms by which TOE affects dextran sulphate sodium (DSS)-induced colitis remain unclear. After DSS-induced colitis were treated with different concentrations of TOE for 8 days, the bodyweight, disease activity index (DAI), colon lengths and pathological scoring were assessed, and histopathological examination was confirmed by HE staining.

Toosendanin alleviates dextran sulfate sodium-induced colitis by inhibiting M1 macrophage polarization and regulating NLRP3 inflammasome and Nrf2/HO-1 signaling.

Toosendanin (TSN), a triterpenoid extracted from the bark of fruit of Melia toosendan Sieb et Zucc, has been proven to have various biological activities including anti-inflammatory activity. But its effects on experimental colitis remain unreported. Herein, we investigated the role and potential mechanisms of TSN in dextran sulfate sodium (DSS) induced colitis in mice.

Network pharmacology-based identification of the protective mechanisms of taraxasterol in experimental colitis.

Background And Aim: Taraxasterol, a pentacyclic-triterpene, has been reported to exert potent anti-inflammatory activity. However, the molecular mechanisms by which taraxasterol attenuates acute experimental colitis (AEC) remain undocumented.

Methods: A network pharmacology approach was used to identify the candidate and collective targets of taraxasterol and acute colitis, and an AEC model was established by oral administration of dextran sulfate sodium (DSS) in mice.