RESUMEN
Sepsis is one of the primary causes of death in intensive care units. Recently, increasing evidence has identified lncRNA HOTAIR is involved in septic cardiomyopathy. However, the potential mechanism underlying HOTAIR on septic cardiomyopathy is still unknown. H9C2 cells were treated with lipopolysaccharide (LPS) after transfection with sh-HOTAIR, sh-Lin28, pcDNA3.1-HOTAIR, and pcDNA3.1-PDCD4. qRT-PCR was used to examine the level of HOTAIR, Lin28, PDCD4, and sepsis-related inflammatory cytokines. Flow cytometric analysis was applied to detect cell apoptosis. The interaction between Lin28 and HOTAIR or PDCD4 was verified by RNA pull-down and RIP assay. HOTAIR levels were interfered by AAV9-sh-HOTAIR in LPS-induced septic cardiomyopathy mice. ELISA analysis was used to evaluate TNF-α, IL-6, and IL-1ß level. Western blot was used to detect the expression of LIN28 and PDCD4 in mouse cardiomyocytes. Echocardiography was used to evaluate the cardiac function. In our study, knockdown of HOTAIR inhibited LPS-induced inflammation and H9C2 cells apoptosis. HOTAIR promoted LPS-induced inflammatory response and apoptosis of H9C2 cells by enhancing PDCD4 stability. RNA pull-down and RIP assay exhibited that Lin28, a highly conserved RNA-binding protein, was combined with HOTAIR and PDCD4. The in vivo experiments verified that the HOTAIR knockdown alleviated the cardiac function injury and secretion of inflammatory factors caused by sepsis. In conclusion, our findings supported that the HOTAIR/Lin28/PDCD4 axis serves as a critical regulator of sepsis, which may open a new direction for the development of sepsis therapeutic.
Asunto(s)
Proteínas Reguladoras de la Apoptosis/biosíntesis , Apoptosis/fisiología , Lipopolisacáridos/toxicidad , Miocitos Cardíacos/metabolismo , ARN Largo no Codificante/biosíntesis , Proteínas de Unión al ARN/biosíntesis , Animales , Apoptosis/efectos de los fármacos , Técnicas de Silenciamiento del Gen/métodos , Inflamación/inducido químicamente , Inflamación/metabolismo , Inflamación/patología , Ratones , Ratones Endogámicos C57BL , Miocitos Cardíacos/efectos de los fármacos , Miocitos Cardíacos/patología , Estabilidad Proteica/efectos de los fármacos , ARN Largo no Codificante/antagonistas & inhibidoresRESUMEN
OBJECTIVE: To evaluate the effects of noninvasive positive pressure ventilation (NPPV) on postoperative pulmonary function recovery in patients receiving thoracic surgeries. METHODS: Fifty thoracic surgical patients were enrolled in this prospective randomized controlled study and divided randomly into conventional treatment group and NPPV group. In the NPPV group, the patients were given NPPV therapy on the basis of conventional treatment. The volume of the residual cavity and the lung function were recorded. RESULTS: At one week after the operation, the changes of lung function parameters were similar between NPPV and control group (P>0.05). CONCLUSIONS: NPPV following thoracic surgeries produces no obvious effects on postoperative pulmonary complications or the lung functions, and bullous resection have less adverse effect than lobectomy on the lung function.