Effects of pulmonary surfactant combined with noninvasive positive pressure ventilation in neonates with respiratory distress syndrome

BACKGROUND Neonatal respiratory distress syndrome(NRDS)is one of the most common diseases in neonatal intensive care units,with an incidence rate of about 7%among infants.Additionally,it is a leading cause of neonatal death in hospitals in China.The main mechanism of the disease is hypoxemia and hypercapnia caused by lack of surfactant AIM To explore the effect of pulmonary surfactant(PS)combined with noninvasive positive pressure ventilation on keratin-14(KRT-14)and endothelin-1(ET-1)levels in peripheral blood and the effectiveness in treating NRDS.METHODS Altogether 137 neonates with respiratory distress syndrome treated in our hospital from April 2019 to July 2021 were included.Of these,64 control cases were treated with noninvasive positive pressure ventilation and 73 observation cases were treated with PS combined with noninvasive positive pressure ventilation.The expression of KRT-14 and ET-1 in the two groups was compared.The deaths,complications,and PaO_(2),PaCO_(2),and PaO_(2)/FiO_(2)blood gas indexes in the two groups were compared.Receiver operating characteristic curve(ROC)analysis was used to determine the diagnostic value of KRT-14 and ET-1 in the treatment of NRDS.RESULTS The observation group had a significantly higher effectiveness rate than the control group.There was no significant difference between the two groups in terms of neonatal mortality and adverse reactions,such as bronchial dysplasia,cyanosis,and shortness of breath.After treatment,the levels of PaO_(2)and PaO_(2)/FiO_(2)in both groups were significantly higher than before treatment,while the level of PaCO_(2)was significantly lower.After treatment,the observation group had significantly higher levels of PaO_(2)and PaO_(2)/FiO_(2)than the control group,while PaCO_(2)was notably lower in the observation group.After treatment,the KRT-14 and ET-1 levels in both groups were significantly decreased compared with the pre-treatment levels.The observation group had a reduction of KRT-14 and ET-1 levels than the control group.ROC curve analysis showed that the area under the curve(AUC)of KRT-14 was 0.791,and the AUC of ET-1 was 0.816.CONCLUSION Combining PS with noninvasive positive pressure ventilation significantly improved the effectiveness of NRDS therapy.KRT-14 and ET-1 levels may have potential as therapeutic and diagnostic indicators.

Gynura procumbens aqueous extract alleviates nonalcoholic steatohepatitis through CFLAR-JNK pathway in vivo and in vitro

Objective:The present work was to investigate the protective effects of the aqueous extract of Gynura procumbens(GPAE)against nonalcoholic steatohepatitis(NASH)in mice and NCTC-1469 cells.Methods:C57 BL/6 J mice were fed with methionine and choline-deficient(MCD)diet and administered simultaneously with GPAE(500 and 1000 mg/kg/d,respectively)by gavage for six weeks.The biomarkers of NASH in serum and liver were determined.NCTC-1469 cells were pretreated with 0.25 mmol/L palmitic acid(PA)plus 0.5 mmol/L oleic acid(OA)for 24 h or treated with adenovirus expressing short-hairpin RNA against CFLAR(Ad-sh CFLAR)for 24 h and then treated with GPAE(80 and 160μg/m L,respectively)for 24 h,and the content of cellular biomarkers of NASH was detected.Results:In mice treated with MCD,GPAE could decrease the levels of serum ALT,AST,the content of hepatic TG,TC and MDA,repress the activities and protein expression of CYP2 E1 and CYP4 A and the phosphorylation of JNK,increase the activities of HO-1,CAT and GSH-Px,up-regulate the m RNA expression of PPARα,FABP5,CPT1α,ACOX,SCD-1,mGPAT,MTTP and the protein expression of CFLAR and NRF2.In NCTC-1469 cells treated with PA and OA,GPAE could decrease the content of cellular TG and ROS,promote the uptake of 2-NBDG,up-regulate the protein expression of CFLAR and NRF2.In NCTC-1469 cells treated with Ad-sh CFLAR,GPAE up-regulated the mRNA and protein expression of CFLAR,down-regulated the phosphorylation of JNK,and increased the protein expression of NRF2 and p IRS1.Conclusion:These results indicated that the activation on CFLAR-JNK pathway might be the main antiNASH mechanism of GPAE,which on the one hand promote theβ-oxidation and efflux of fatty acids in liver,and finally reduce hepatic lipid accumulation,on the other hand increase the activities of antioxidant enzymes and inhibit the activities of ROS generation enzymes by activating NRF2,and therefore attenuates hepatic oxidative stress damage.