RÉSUMÉ
Objective:To investigate the effect of glabridin on neutrophil extracellular traps (NETs) formation and pyroptosis in rats with sepsis-induced lung injury.Methods:Twenty-four male Wistar rats were divided into three groups according to the random number table method. The sepsis group was established by cecal ligation and puncture (CLP). The Glabridin group underwent CLP and glabridin gavage (30 mg/kg)(CLP+GLA). The sham operation group underwent cecal exploration, and only the abdomen was closed after cecal turning(Sham). After 12 hours, plasma、alveolar lavage fluid and lung tissue samples were taken for detection . Then, protein content of the alveolar lavage fluid was determined; The wet/dry weight(W/D) ratio of the lung tissue was determined; The pathological changes in lung tissue were observed after hematoxylin-eosin (HE) staining. The levels of NETs marker MPO-DNA complex and related inflammatory factors IL-18 and IL-1β in plasma were detected by enzyme-linked immunosorbent assay. The changes of Caspase-1and Cleaved-caspase-1 protein in lung tissue were detected by Western blot.Results:The total protein concentration of alveolar lavage fluid was significantly higher in the sepsis group compared with the Sham group ( P<0.01), and it decreased in the glabridin group compared with the sepsis group ( P<0. 05). Significant aggravation of pulmonary edema in the sepsis group, and the glabridin group reduced pulmonary edema compared with the sepsis group.The pathological results of lung tissue under the light microscope showed: The structure of lung tissue in the Sham group was normal, and the alveoli were clear; In the sepsis group, the alveolar wall was thickened widely and inflammatory cells infiltrated obviously; Compared with the sepsis group, the lung tissue injury was significantly reduced in the light licorice group. The enzyme-linked immunosorbent assay results showed that the levels of NETs marker MPO-DNA complex and inflammatory factors IL-18 and IL-1β in the plasma of the sepsis group were significantly higher than those in the Sham group ( P<0.001). The levels of NETs marker MPO-DNA complex and inflammatory factors IL-18 and IL-1β in the glabridin group were significantly lower than those in the sepsis group (MPO-DNA: P<0. 01; IL-18、IL-1β: P<0.05) . Western blot Technical results showed that the expression of Caspase-1 and Cleaved-caspase-1 protein positive signal was significantly enhanced in the lung tissue of the rats in the sepsis group compared with the Sham group; the distribution of Caspase-1 positive cells in the lung tissue of the sepsis + glabridin group was similar to that of the Sham group, and the expression of Cleaved-caspase-1 positive signal was higher than that of the Sham group. Conclusions:Glabridin can effectively reduce lung inflammation and play a protective role in lung injury in septic rats by inhibiting NETs production and pyroptosis.
RÉSUMÉ
Nasopharyngeal carcinoma (NPC) is one of the most common malignant tumors of the head and neck region. NPC has the characteristics of insidious onset, strong invasiveness and early lymph node metastasis. A variety of signaling pathways play a role in the invasion and metastasis of nasopharyngeal carcinoma, but the specific mechanism has not yet been fully elucidated. Recent studies have found that DNA methylation of nasopharyngeal carcinoma-related genes can affect the invasion and metastasis of nasopharyngeal carcinoma through a variety of signaling pathways including Wnt/β-catenin, PI3K/AKT and MAPK signaling pathways. This article reviews the specific mechanism of DNA methylation affecting the invasion and metastasis of nasopharyngeal carcinoma through the above-mentioned signaling pathways.
RÉSUMÉ
The use of the breathing machine undoubtedly represents the progress in the field of respiratory insufficien-cy treatment,although it has saved many lives,but its side effects are also as everyone knows. Ventilator-associated pneumonia is the most important complication of mechanical ventilation ,it can make the cost of hospitalization and the mortality of patients increased significantly. Pathological biopsy and histological training as the “gold standard ”for di-agnosis of ventilator-associated pneumonia ,but it is the invasive operation and it difficult to fully implement , recently the diagnosis is still controversial. Emerged in recent years the biomarkers for the diagnosis research , but the diver-gence of the corresponding research conclusion is wide. Now , biomarkers that would be useful for diagnosis of ventila-tor-associated pneumonia are reviewed so as to it can improve people ’s understanding of the value of biomarkers in the diagnosis of ventilator-associated pneumonia.