RESUMO
The soluble ectodomain of fibroblast growth factor receptor-IIIc (sFGFR2c) is able to bind to fibroblast growth factor (FGF) ligands and block the activation of the FGF-signaling pathway. In this study, sFGFR2c inhibited lung fibrosis dramatically in vitro and in vivo. The upregulation of α-smooth muscle actin (α-SMA) in fibroblasts by transforming growth factor-ß1 (TGF-ß1) is an important step in the process of lung fibrosis, in which FGF-2, released by TGF-ß1, is involved. sFGFR2c inhibited α-SMA induction by TGF-ß1 via both the extracellular signal-regulated kinase 1/2 (ERK1/2) and Smad3 pathways in primary mouse lung fibroblasts and the proliferation of mouse lung fibroblasts. In a mouse model of bleomycin (BLM)-induced lung fibrosis, mice were treated with sFGFR2c from d 3 or d 10 to 31 after BLM administration. Then we used hematoxylin and eosin staining, Masson staining and immunohistochemical staining to evaluate the inhibitory effects of sFGFR2c on lung fibrosis. The treatment with sFGFR2c resulted in significant attenuation of the lung fibrosis score and collagen deposition. The expression levels of α-SMA, p-FGFRs, p-ERK1/2 and p-Smad3 in the lungs of sFGFR2c-treated mice were markedly lower. sFGFR2c may have potential for the treatment of lung fibrosis as an FGF-2 antagonist.
Assuntos
Actinas/antagonistas & inibidores , Fibrose Pulmonar/metabolismo , Fibrose Pulmonar/patologia , Receptor Tipo 2 de Fator de Crescimento de Fibroblastos/química , Receptor Tipo 2 de Fator de Crescimento de Fibroblastos/metabolismo , Actinas/metabolismo , Animais , Bleomicina , Proliferação de Células/efeitos dos fármacos , Células Cultivadas , Modelos Animais de Doenças , Ativação Enzimática/efeitos dos fármacos , Fator 2 de Crescimento de Fibroblastos/metabolismo , Fator 2 de Crescimento de Fibroblastos/farmacologia , Fibroblastos/efeitos dos fármacos , Fibroblastos/metabolismo , Fibroblastos/patologia , Regulação da Expressão Gênica/efeitos dos fármacos , Humanos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Pneumonia/complicações , Pneumonia/genética , Pneumonia/patologia , Ligação Proteica/efeitos dos fármacos , Isoformas de Proteínas/metabolismo , Estrutura Terciária de Proteína , Fibrose Pulmonar/enzimologia , Fibrose Pulmonar/genética , Proteínas Smad/metabolismo , Ressonância de Plasmônio de Superfície , Fator de Crescimento Transformador beta1/farmacologiaRESUMO
Objective To investigate the relationship between dynamic changes of plasma D-dimer and survival rate of the esophageal carcinoma patients pre-and post-operation.Methods 30 cases of normal control group,160 cases of esophageal cancer group( including operation cases n =112),with the gold standard method for the determination of plasma D-dimer.Results There was a link between the level of D-dimer,TNM staging,lymph node metastasis and tumor size in esophageal carcinoma patients.Compared with the preoperation,the plasma D-dimer is significantly elevated 2 years later( t =7.35,P ＞ 0.05 ).Conclusion Before or after the operation,dynamic changes of plasma D-dimer had a relationship with short-term survival rate.
RESUMO
Objective To study the diagnosis and treatment results of the traumatic perforation of the esophagus.Methods Retrospective analysis was performed in 19 cases with the traumatic perforation of the esophagus hospitalized.Results Treatment options ranged from aggressive to conservative management.Repair of esophageal perforation was performed in 9 cases,cervical drainage in 2 cases and conservative treatment in 8 cases.17 cases recovered from the disease,making up 89.5%the mortality rate was 10.5%.Conclusion In order to increase the recovery rate and decrease the mortality.it is important to diagnose and treat the disease in it's early phases.
RESUMO
Objectives:Dose-response effect of nicorandil cardioplegia at various concentrations was studied to optimize its myocardial protective effect.Methods:Forty-eight isolated working rat hearts were divided into 6 groups randomly.They were group A:control (depolarized cardiac arrest with St.Thomas solution No.2),group B,C,E,F and G:hyperpolarized cardiac arrest (nicorandil concentration were 25,50,100,125 and 150μmol/L respectively).The hearts underwent a 120-minute hypothermic arrest (15±1)℃ with cardioplegia (40 ml/kg) and reinfused with cardioplegia (40 ml/kg) at interval of 30 minutes.Mechanical arrest time,cardiac functional recoveries,myocardial content of malondialdehyde (MDA) and ultrastructure were measured.Results:The protective effect of nicorandil cardioplegia was dose-related.Conclusions:The optimal concentration of nicorandil in cardiplegia may be 100μmol/L for myocardial protection.
RESUMO
AIM:To determine the effect of rhBMP2 on the migration of human breast cancer cells MCF-7. METHODS:MCF-7 was induced by rhBMP2 (30 ?g/L) for 24 h. Atomic force microscopy (AFM) was used to observe the changes in cell morphology. Cell migration and invasion abilities were assayed by scratch healing and transwell experiments. RESULTS:The formation of lamellipodia and cell polarity together with increased cell length were observed in the cells treated with rhBMP2,whereas lamellipodia of cells in control group were not obvious and the majority of cells tended to be rounder with shorter cell diameter. Compared to control group,scratch healing and transwell experiments showed that the migration and invasion capacity of rhBMP2-induced MCF-7 cells was markedly enhanced. CONCLUSION:rhBMP2 induces human breast cancer cell MCF-7 to present the phenotype of migration and enhances the invasion capacity.
