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Objective To investigate whether levosimendan can inhibit the apoptosis of C2C12 cells induced by lipopolysaccharide(LPS)through the PTEN/Akt pathway.Methods C2C12 cells were randomly divided into four groups:blank control group,control group comprising cells treated with levosimendan only,LPS-treated group,and a group comprising cells pretreated with levosimendan for 24 h a subsequently treated with LPS for 48 h.The survival rate of C2C12 cells was determined via the CCK-8 method,and cell apoptosis was assessed via Hoechst 33342 staining.The mRNA and protein expression levels of PTEN/Akt pathway components were evaluated via RT-qPCR and Western blotting,respectively.C2C12 cells were also transfected with siRNA to knockdown the PTEN gene,and the effect on the protein expression of apoptotic pathway components was determined.Results Levosimendan increased the survival rate and decreased the apoptosis rate of C2C12 cells after LPS treatment.PTEN gene expression was inhibited by siRNA and the mRNA and protein levels of PTEN/Akt signaling pathway components changed correspondingly.Furthermore,the apoptosis rate of C2C12 cells decreased.Conclusion Levosimendan can inhibit LPS-induced C2C12 cell apoptosis via the PTEN/Akt pathway.
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Objective To Analyze the etiology and antibiotic susceptibility in exacerbated bronchiectasis, and guide rational drug use in clinic. Methods Pathogenic microorganism culture and drug sensitivity of sputum samples of 496 cases were collected from 2015 to 2016 in Shengjing Affiliated Hospital, China Medical University. The Excel software was used to analyze the screening data and the SPSS 22.0 was used for statistical analysis to obtain the drug resistance of the bacteria to the commonly used antibiotics. Results In 469 patients, there were 551 pieces of sputum , with 198 strains positive bacterium. Positive rate was 35.93%(198/551), and bacterium was 171 strains (86.36%). Bacteria of top three positive rate was 86 strains of Pseudomonas aeruginosa (50.29%), 54 strains of Acinetobacter baumannii (31.58%) and 10 strains of Klebsiella pneumoniae (5.85%). The resistance rate of Acinetobacter baumannii and Pseudomonas aeruginosa was higher, and other pathogens also showed various degrees of tolerance to antibiotic. Conclusions The pathogens in patients with acute exacerbation of bronchiectasis are Gram-negative bacteria. Considering the characters of Pseudomonas aeruginosa, it is not suggested to use cephalosporin of the third and fourth generation in treating Pseudomonas aeruginosa. Clinical selection of antibiotics should combine with the disease characteristics of patients in our hospital.
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<p><b>OBJECTIVE</b>To determine if aquaporin1 (AQP1) and aquaporin5 (AQP5) are expressed in the alveolar capillary membrane in rats. Moreover, to investigate the alteration of AQP1 and AQP5 in acute injured lungs.</p><p><b>METHODS</b>The distribution of AQP1 and AQP5 in alveolar capillary membrane were investigated by immunohistochemistry and immunoelectron microscopy with affinity-purified antibodies to human AQP1 and AQP5. To study the possibility that alveolar capillary membrane AQP1 and AQP5 undergo altered regulation, we established a rat model using alveolar instillation of lipopolysaccharide (LPS).</p><p><b>RESULTS</b>Immunolabelling showed AQP1 was stained primarily in the microvascular endotheli a of normal lungs, while AQP5 was expressed in type I pneumocytes. Immunohisto chemical analysis showed a significant decrease in the expression of AQP1 and AQP5 in injured lungs at 4h-48h after LPS instillation. AQP1 protein was resumed partly at 24h after LPS instillation and steroid administration, whereas AQP5 was unchanged.</p><p><b>CONCLUSION</b>The decreased expressions of AQP1 and AQP5 in injured lungs suggest that both of them may play a role in abnormal fluid transportation.</p>
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Animais , Masculino , Ratos , Aquaporina 1 , Aquaporina 5 , Aquaporinas , Imuno-Histoquímica , Lipopolissacarídeos , Toxicidade , Pulmão , Metabolismo , Proteínas de Membrana , Microscopia Imunoeletrônica , Ratos Sprague-Dawley , Síndrome do Desconforto Respiratório , Metabolismo , PatologiaRESUMO
0.05). In comparison to control group (26.5%?14.3%), the fatigue index (FI) decreased remarkably in CMV+PEEP group (12.2%?6.4%, P