RESUMEN
BACKGROUND: Helicobacter pylori (H. pylori) infection is closely associated with gastrointestinal diseases. Our preliminary studies have indicated that H. pylori infection had a significant impact on the mucosal microbiome structure in patients with gastric ulcer (GU) or duodenal ulcer (DU). AIM: To investigate the contributions of H. pylori infection and the mucosal microbiome to the pathogenesis and progression of ulcerative diseases. METHODS: Patients with H. pylori infection and either GU or DU, and healthy individuals without H. pylori infection were included. Gastric or duodenal mucosal samples was obtained and subjected to metagenomic sequencing. The compositions of the microbial communities and their metabolic functions in the mucosal tissues were analyzed. RESULTS: Compared with that in the healthy individuals, the gastric mucosal microbiota in the H. pylori-positive patients with GU was dominated by H. pylori, with significantly reduced biodiversity. The intergroup differential functions, which were enriched in the H. pylori-positive GU patients, were all derived from H. pylori, particularly those concerning transfer RNA queuosine-modification and the synthesis of demethylmenaquinones or menaquinones. A significant enrichment of the uibE gene was detected in the synthesis pathway. There was no significant difference in microbial diversity between the H. pylori-positive DU patients and healthy controls. CONCLUSION: H. pylori infection significantly alters the gastric microbiota structure, diversity, and biological functions, which may be important contributing factors for GU.
Asunto(s)
Úlcera Duodenal , Mucosa Gástrica , Microbioma Gastrointestinal , Infecciones por Helicobacter , Helicobacter pylori , Úlcera Gástrica , Humanos , Infecciones por Helicobacter/microbiología , Helicobacter pylori/aislamiento & purificación , Helicobacter pylori/genética , Úlcera Duodenal/microbiología , Úlcera Duodenal/diagnóstico , Masculino , Femenino , Persona de Mediana Edad , Mucosa Gástrica/microbiología , Mucosa Gástrica/patología , Úlcera Gástrica/microbiología , Adulto , Estudios de Casos y Controles , Anciano , Metagenómica/métodos , Duodeno/microbiología , Disbiosis/microbiologíaRESUMEN
<p><b>OBJECTIVE</b>To study the suppressive role of emodin on the growth and its effect on the proliferation cycle and apoptotic gene of human lung adenocarcinoma cell line Anip 973.</p><p><b>METHODS</b>The survival rate and the inhibitory rate of Anip 973 cell in vitro were detected by MTT colorimetric assay and cell growth curve assay at different time points under different concentration of emodin; the cell proliferation cycle and the apoptotic rate were examined with flow cytometry analysis, and Caspase-3 protein expression was measured by immunoblotting assay.</p><p><b>RESULTS</b>Emodin inhibited the proliferation of Anip 973 cell at G0/G1 phase, decreased the cell ratio at S phase and activated the Caspase-3 protein. It suppressed the growth of tumor cells and raised the apoptotic rate in a concentration and time depending manner in a certain extent.</p><p><b>CONCLUSION</b>Emodin could suppress the proliferation of Anip 973 cell, and its mechanism of anticancer effect may be through activating Caspase-3, to induce apoptosis and block cell cycle.</p>
Asunto(s)
Anciano , Humanos , Masculino , Adenocarcinoma , Metabolismo , Patología , Antineoplásicos Fitogénicos , Farmacología , Apoptosis , Western Blotting , Caspasa 3 , Metabolismo , Ciclo Celular , Línea Celular Tumoral , Proliferación Celular , Relación Dosis-Respuesta a Droga , Emodina , Farmacología , Neoplasias Pulmonares , Metabolismo , PatologíaRESUMEN
<p><b>OBJECTIVE</b>To investigate the anti-tumor mechanisms of emodin on human lung adenocarcinoma cell line Anip973 (LACC).</p><p><b>METHODS</b>The influence of emodin of different concentration at different time on LACC proliferation were determined and compared using MTT colorimeric assay and cell growth curve assay. And the cell apoptotic rate was determined by flow cytometry and analyzed with electronic microscope.</p><p><b>RESULTS</b>In a certain range, the higher concentration and longer acting time of emodin could induce the stronger inhibitory effect on tumor cell growth and the higher apoptotic rate. The proliferation inhibitory rate reached 90% after LACC being treated with emodin 60 micromol/L for 72h.</p><p><b>CONCLUSION</b>Emodin can significantly inhibit proliferation of human LACC, showing dose-effect and time-effect relationship.</p>