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1.
Acta cir. bras ; 32(7): 568-575, July 2017. tab
Article in English | LILACS | ID: biblio-886221

ABSTRACT

Abstract Purpose: To evaluate the possibility of using peripheral-blood presurfactant protein B (Pro-SFTPB) for screening non-small cell lung cancer (NSCLC). Methods: A total of 873 healthy volunteers and 165 lung cancer patients hospitalized in the Fifth People's Hospital of Dalian were tested Pro-SFTPB once every half year from January 2014 to September 2015. The healthy volunteers were also conducted spiral computed tomography (CT) examination once every year. The data were then com-pared and statistically analyzed. Results: The positive expression rate of Pro-SFTPB in NSCLC was significantly higher than that in healthy volunteers, and significantly higher in lung adenocarcinoma than in squamous cell carcinoma; additionally, the expression rate was increased with the in-crease of smoking index, and the intergroup differences showed statistical signifi-cance (p≤0.05). The positive rate of newly diagnosed lung cancer was 29.55%, higher than healthy volunteers (22.34%), but there was no significant difference (p>0.05). Conclusion: Pro-SFTPB is over expressed in non-small cell lung cancer, especially in lung adeno-carcinoma, but it can't be used as a clinical screening tool for lung cancer.


Subject(s)
Humans , Male , Female , Aged , Protein Precursors/blood , Carcinoma, Non-Small-Cell Lung/diagnosis , Carcinoma, Non-Small-Cell Lung/blood , Pulmonary Surfactant-Associated Proteins/blood , Lung Neoplasms/diagnosis , Lung Neoplasms/blood , Biomarkers, Tumor/blood , Case-Control Studies , Mass Screening , Sensitivity and Specificity
2.
Yonsei Medical Journal ; : 823-828, 2017.
Article in English | WPRIM | ID: wpr-81889

ABSTRACT

PURPOSE: Pulmonary surfactants for preterm infants contain mostly animal-derived surfactant proteins (SPs), which are essential for lowering surface tension. We prepared artificial pulmonary surfactants using synthetic human SP analogs and performed in vitro and in vivo experiments. MATERIALS AND METHODS: We synthesized peptide analogues that resemble human SP-B (RMLPQLVCRLVLRCSMD) and SP-C (CPVHLKRLLLLLLLLLLLLLLLL). Dipalmitoylphosphatidylcholine (DPPC), phosphatidylglycerol (PG), and palmitic acid (PA) were added and mixed in lyophilized to render powdered surfactant. Synsurf-1 was composed of DPPC:PG:PA:SP-B (75:25:10:3, w/w); Synsurf-2 was composed of DPPC:PG:PA:SP-C (75:25:10:3, w/w); and Synsurf-3 was composed of DPPC:PG:PA:SP-B:SP-C (75:25:10:3:3, w/w). We performed in vitro study to compare the physical characteristics using pulsating bubble surfactometer and modified Wilhelmy balance test. Surface spreading and adsorption test of the surfactant preparations were measured. In vivo test was performed using term and preterm rabbit pups. Pressure-volume curves were generated during the deflation phase. Histologic findings were examined. RESULTS: Pulsating bubble surfactometer readings revealed following minimum and maximum surface tension (mN/m) at 5 minutes: Surfacten® (5.5±0.4, 32.8±1.6), Synsurf-1 (16.7±0.6, 28.7±1.5), Synsurf-2 (7.9±1.0, 33.1±1.6), and Synsurf-3 (7.1±0.8, 34.5±1.0). Surface spreading rates were as follows: Surfacten® (27 mN/m), Synsurf-1 (43 mN/m), Synsurf-2 (27 mN/m), and Synsurf-3 (27 mN/m). Surface adsorption rate results were as follows: Surfacten® (28 mN/m), Synsurf-1 (35 mN/m), Synsurf-2 (29 mN/m), and Synsurf-3 (27 mN/m). The deflation curves were best for Synsurf-3; those for Synsurf-2 were better than those for Surfacten®. Synsurf-1 was the worst surfactant preparation. Microscopic examination showed the largest aerated area of the alveoli in the Synsurf-3 group, followed by Synsurf-1 and Surfacten®; Synsurf-2 was the smallest. CONCLUSION: Synsurf-3 containing both SP-B and SP-C synthetic analogs showed comparable and better efficacy than commercially used Surfacten® in lowering surface tension, pressure-volume curves, and tissue aerated area of the alveoli.


Subject(s)
1,2-Dipalmitoylphosphatidylcholine , Adsorption , Animal Experimentation , Animals , Humans , In Vitro Techniques , Infant, Newborn , Infant, Premature , Palmitic Acid , Pulmonary Surfactant-Associated Proteins , Pulmonary Surfactants , Reading , Surface Tension
3.
Article in English | WPRIM | ID: wpr-185148

ABSTRACT

Respiratory distress syndrome (RDS) among preterm infants is typically due to a quantitative deficiency of pulmonary surfactant. Aside from the degree of prematurity, diverse environmental and genetic factors can affect the development of RDS. The variance of the risk of RDS in various races/ethnicities or monozygotic/dizygotic twins has suggested genetic influences on this disorder. So far, several specific mutations in genes encoding surfactant-associated molecules have confirmed this. Specific genetic variants contributing to the regulation of pulmonary development, its structure and function, or the inflammatory response could be candidate risk factors for the development of RDS. This review summarizes the background that suggests the genetic predisposition of RDS, the identified mutations, and candidate genetic polymorphisms of pulmonary surfactant proteins associated with RDS.


Subject(s)
Genetic Predisposition to Disease , Humans , Infant, Newborn , Infant, Premature , Polymorphism, Genetic , Pulmonary Surfactant-Associated Proteins , Pulmonary Surfactants , Risk Factors , Twins
4.
Chinese Journal of Pediatrics ; (12): 843-846, 2012.
Article in Chinese | WPRIM | ID: wpr-348525

ABSTRACT

<p><b>OBJECTIVE</b>To explore the prevalence of pulmonary surfactant associated pathway genes functional variants in Chinese population.</p><p><b>METHOD</b>Using a cohort of 258 mixed ethnic population of Han and Zhuang, we pooled DNA samples from 146 term male infants and 112 term female infants and then used an Ill umina next generation sequencing platform to perform the complete exonic resequencing in 6 target genes:surfactant protein-B (SFTPB), surfactant protein-C (SFTPC), ATP-binding cassette transporter A3 (ABCA3), lysophospholipid acyltransferase 1 (LPCAT1), choline phosphotransferase 1 (CHPT1), phosphate cytidylyltransferase 1, choline, beta (PCYT1B). Collapsing methods was used to determine the functional allele frequency.</p><p><b>RESULT</b>(1) Altogether, 128 variants were found, including 44 synonymous variants, 66 nonsynonymous variants and 18 insertions-deletions. Of these, 28 variants were predicted to alter protein function. Two of these variants were seen twice, the rest variants were only seen once, for a total of 30 functional alleles; (2) ABCA3 had the most functional variants in both male and female groups with the minor allele frequencies of 0.014 (1.4%) and 0.04 (4%), respectively. The total functional allele frequencies of 6 genes were 0.041 (4.1%) and 0.08 (8%) in the two groups, respectively (P = 0.06).</p><p><b>CONCLUSION</b>(1) Functional variants in pulmonary surfactant associated pathway genes are present in the mixed Han-Zhuang population. (2) ABCA3 contained the most functional variants suggesting that ABCA3 could contribute significantly to neonatal respiratory distress syndrome and other lung disease.</p>


Subject(s)
1-Acylglycerophosphocholine O-Acyltransferase , Genetics , Metabolism , ATP-Binding Cassette Transporters , Genetics , Asians , Ethnology , Genetics , China , Ethnology , Female , Gene Frequency , Genetic Association Studies , Genetic Predisposition to Disease , Genetic Variation , Genotype , Humans , Infant, Newborn , Male , Pulmonary Surfactant-Associated Protein C , Genetics , Pulmonary Surfactant-Associated Proteins , Genetics , Respiratory Distress Syndrome, Newborn , Ethnology , Genetics
5.
Article in Chinese | WPRIM | ID: wpr-242767

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the change of lung surfactant protein (SP) A,B,C,D of rats following silica dust exposure in order to provide the evidences for the early diagnosis indices or therapy of silicosis.</p><p><b>METHODS</b>60 male SD rats were randomly divided into silica group, and corresponding controls group. Rats in silica group were administrated 1 ml silica solution by intratracheal instillation at dose of 50 mg/ml. Rats in control group were administrated the same amount saline. At 3rd, 7th, 14th, 21st, 28th after silica exposure, serum and bronchoalveolar lavage fluid (BALF) samples were obtained. The concentration of SP-A, SP-B, SP-C, SP-D in serum and BALF were measured by using enzyme immunoassay (ELISA). Meanwhile the levels of total anti-oxidative activity (T-AOC) and hydroxyproline (HYP) in lung tissue were also detected. The pathology of lung tissue was conducted.</p><p><b>RESULTS</b>Compared with control group, SP-A concentration in BALF of silica exposed rat for 3, 14, 21, 28d was significant lower and SP-D concentration in BALF of silica exposed rat for all time points was also lower. The differences were significant (P < 0.05). Meanwhile SP-B level in 7, 14, 21, 28 d silica exposed rats BALF and SP-C level in 14, 21, 28 d silica exposed rats markedly decreased (P < 0.05). In addition compared with control group, SP-A, SP-B and SP-C concentration in serum of silica exposed rat were higher when SP-A for 14, 21, 28 d silica exposure, SP-B for 7, 14, 21 d silica exposure and Sp-C for 7, 14, 21, 28 d exposure. And all difference were significant (P < 0.05). As silica exposure time increased, SP-C concentration in serum showed an increase trend, which showed a time-response relationship (r = 0.618, P = 0.042). However, SP-D concentration in serum of rat for 7, 14, 21, 28d silica exposure were significant lower than that of control group (P < 0.005). And there was a decrease trend with time point exposure regarding of SP-D (r = -0.731, P = 0.016). The HYP content in lung tissue of experiment rats increased at 3rd, 7th, 14th, 21st and 28th day time point and The T-AOC activity in lung tissue decrease at, 7th, 14th, 21st and 28th day time point. The differences were significant (P < 0.05). There was a positive correlation (P = 0.803, P = 0.045) between SP-C in BALF and HYP of silica exposed rats and a negative correlation between SP-D in BALF and HYP (r = -0.867, P = 0.033). No significant correlation were seen between SP-A, SP-B BALF and HYP (y = 0.416, P = 0.28; r = 0.592, P = 0.071). SP-C concentration in BALF and serum all showed an increased trend and a positive correlation was seen (r = 0.539, P = 0.046). The same decrease trend was seen between SP-D in BALF and serum and correlation value was 0.870 (P = 0.034).</p><p><b>CONCLUSION</b>The silica exposure did cause the change of SP content both in BALF and serum. The SP-C and SP-D content in serum might be served as an early effective biomarker of silicosis.</p>


Subject(s)
Animals , Bronchoalveolar Lavage Fluid , Male , Pulmonary Fibrosis , Metabolism , Pathology , Pulmonary Surfactant-Associated Proteins , Metabolism , Rats , Rats, Sprague-Dawley , Silicon Dioxide , Silicosis , Metabolism , Pathology
6.
Rev. Inst. Med. Trop. Säo Paulo ; 53(4): 235-238, July.-Aug. 2011. graf
Article in English | LILACS | ID: lil-598607

ABSTRACT

Surfacen® is an exogenous natural lung surfactant, composed by phospholipids and hydrophobic proteins, which is applied successfully in Newborn Respiratory Distress Syndrome. In this paper, in vitro activity of Surfacen® against Leishmania amazonensis is described. The product showed activity against the amastigote form found in peritoneal macrophages from BALB/c mice, with an IC50 value of 17.9 ± 3.0 µg/mL; while no toxic effect on host cell was observed up to 200 µg/mL. This is the first report about the antileishmanial activity of Surfacen®.


Surfacen® es un surfactante natural exógeno extraído del pulmón, formado por fosfolípidos y proteínas hidrofóbicas, el cual es aplicado con éxito en el Síndrome de Distrés Respiratorio en Niños Recién Nacidos. En este trabajo, se describe la actividad in vitro del Surfacen® contra Leishmania amazonensis. El producto mostró actividad frente a amastigotes que se encuentran en macrófagos peritoneales de ratón BALB/c, con una CI50 de 17.9 ± 3.0 µg/mL, mientras no se observaron efectos tóxicos sobre la célula hospedera hasta 200 µg/mL. Este estudio constituye el primer reporte sobre la actividad antileishmania del Surfacen®.


Subject(s)
Animals , Mice , Antiprotozoal Agents/pharmacology , Leishmania mexicana/drug effects , Phospholipids/pharmacology , Pulmonary Surfactant-Associated Proteins/pharmacology , Mice, Inbred BALB C , Macrophages, Peritoneal/parasitology , Parasitic Sensitivity Tests , Pulmonary Surfactants/pharmacology
7.
São Paulo; s.n; 2011. [90] p. ilus, tab, graf.
Thesis in Portuguese | LILACS | ID: lil-609496

ABSTRACT

Alguns estudos sugerem que as pequenas vias aéreas têm um papel importante na fisiopatologia da lesão pulmonar aguda/ síndrome do desconforto respiratório agudo (LPA/SDRA). O epitélio respiratório que reveste as vias aéreas é capaz de liberar mediadores inflamatórios e está relacionado ainda com a produção de surfactante nas vias aéreas. Até o presente momento, existem poucos estudos que avaliaram se estas funções do epitélio que reveste as pequenas vias aéreas encontram-se alteradas na SDRA. No presente estudo, nós mensuramos a expressão da proteína de surfactante (PS) A e PS-B, a expressão de citocinas inflamatórias interleucina (IL)-6 e IL-8, e um índice de apoptose do epitélio que reveste as pequenas vias aéreas de pacientes com SDRA que foram submetidos a autópsia e comparamos estes resultados com os de indivíduos controle. Foram incluídos no estudo pulmões de autópsia de 31 pacientes com SDRA (PaO2/FiO2200, 45±14 anos, 16 homens) e 11 controles (52±16 anos, 7 homens). A expressão de IL-6, IL-8, PS-A e PS-B no epitélio das pequenas vias aéreas (diâmetro2.0mm) foi verificada através de reações de imunohistoquímica e análise de imagem. O índice de apoptose epitelial das vias aéreas foi avaliado através do método de TUNEL e da expressão de FAS/FASL. Avaliou-se ainda a densidade de células inflamatórias positivas para IL-6 e IL-8 na parede das pequenas vias aéreas. As vias aéreas dos pacientes com SDRA apresentaram maior expressão epitelial de IL-8 (p=0,006) e maior densidade de células inflamatórias expressando IL-6 (p=0,004) e IL-8 (p<0,001) quando comparadas com o grupo controle. Não houve diferenças na expressão epitelial de PS-A e PS-B ou no índice de apoptose epitelial entre os grupos SDRA e controle. Nossos resultados mostram que as pequenas vias aéreas participam da inflamação pulmonar de pacientes com SDRA, caracterizada pelo aumento na expressão de interleucinas próinflamatórias tanto em células inflamatórias da parede da via aérea quanto no epitélio.


Recent studies suggest a role for distal airway injury in the pathophysiology of human ALI/ARDS. The epithelium lining the airways modulates airway function secreting a large number of molecules such as surfactant components and inflammatory mediators. So far, there is little information on how these secretory functions of the small airways are altered in ARDS. In the present study we assessed the airway expression of surfactant protein (SP) A and SP B, the expression of inflammatory cytokines IL-6 and IL-8, and an index of airway epithelial apoptosis of patients with ARDS submitted to autopsy and compared the results with those of control subjects. We studied autopsy lungs of 31 ARDS patients (PaO2/FiO2200, 45±14 years, 16 males) and 11 controls (52±16 years, 7 males). Using immunohistochemistry and image analysis, we quantified the expression of IL-6, IL-8 and SP-A and SP-B in the epithelium of small airways (diameter2.0mm). Airway epithelial apoptosis index was obtained with the TUNEL assay and FAS/FASL expression. We also quantified the density of inflammatory cells expressing IL-6 and IL-8 within the small airway walls. ARDS airways showed an increase in the epithelial expression of IL-8 (p=0.006) and an increased density of inflammatory cells expressing IL-6 (p=0.004) and IL-8 (p<0.001) when compared to controls. There were no differences in SP-A and SP-B epithelium expression or in epithelial apoptosis index between ARDS and controls. Our results show that the distal airways are involved in ARDS lung inflammation with higher expression of pro-inflammatory interleukins in both airway epithelial and inflammatory cells. Our results also suggest that apoptosis is not a major mechanism of airway epithelial cell death in ARDS.


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Apoptosis , Cytokines , Pulmonary Surfactant-Associated Proteins , Respiratory Distress Syndrome , Respiratory Mucosa , Epithelial Cells
8.
Chinese Journal of Burns ; (6): 372-374, 2008.
Article in Chinese | WPRIM | ID: wpr-257478

ABSTRACT

Inhalation injury is a major contributor to the morbidity and mortality associated with serious burns. The improvement in the understanding of smoke inhalation injury had been obtained in the last half century in China. The models of steam and smoke inhalation injury had been reproduced and a series of experimental studies had been performed. It was found that chemical bronchiotracheitis, pulmonary edema and alveolar collapse (atelectasis) were the primary pathologic findings after inhalation injury. The second inflammatory response would play an important role in the development of acute respiratory failure. The roles of some cytokines, inflammatory cells and pulmonary surfactants in the development of inhalation injury had been elucidated. The etiologic factors and the pathophysiologic changes in inhalation injury had been illustrated clearly. These basic science investigations had led to the advances in protective strategies for the complications of inhalation injury. Now the morbidity and mortality of inhalation injury have decreased markedly in China.


Subject(s)
Burns, Inhalation , Therapeutics , China , High-Frequency Ventilation , Humans , Pulmonary Surfactant-Associated Proteins , Smoke Inhalation Injury , Therapeutics
9.
Article in English | WPRIM | ID: wpr-814164

ABSTRACT

OBJECTIVE@#To investigate the distribution of pulmonary surfactant protein A (SP-A) like molecules and the bridge of frontier host defense and adaptive immune response cell of CD68 positive macrophages in inflammatory bowel disease (IBD).@*METHODS@#Surgical specimens derived from involved areas and normal area of the colon with Crohn disease (CD) and ulcerative colitis (UC) were obtained from Department of Pathology, Rhode Island Hospital, Brown University Medical Center. The distribution of SP-A like molecule in intestine of IBD was detected by immunohistochemistry.@*RESULTS@#SP-A like molecule located in epithelia of intestine, the surface of intestine villi, blood vessels of connective tissue, and some inflammatory cells. The number of macrophages with both SP-A like molecule and CD68 positive was dramatically increased in the inflammatory area than the normal area. Some CD68 positive macrophages expressed SP-A like immunoreactivity by immunofluorescence double labeling.@*CONCLUSION@#SP-A is an important host defense molecule in lung, and SP-A expression in large intestine may reflect a close relation between 2 organs in immune response towards inflammation.


Subject(s)
Antigens, CD , Metabolism , Antigens, Differentiation, Myelomonocytic , Metabolism , Colitis, Ulcerative , Allergy and Immunology , Metabolism , Colon , Metabolism , Crohn Disease , Allergy and Immunology , Metabolism , Humans , Immunohistochemistry , Inflammatory Bowel Diseases , Allergy and Immunology , Metabolism , Macrophages , Allergy and Immunology , Metabolism , Pulmonary Surfactant-Associated Proteins , Genetics , Metabolism
10.
Clinics ; 62(2): 181-190, Apr. 2007. ilus
Article in English | LILACS | ID: lil-449659

ABSTRACT

Pulmonary surfactant is a substance composed of a lipoprotein complex that is essential to pulmonary function. Pulmonary surfactant proteins play an important role in the structure, function, and metabolism of surfactant; 4 specific surfactant proteins have been identified: surfactant proteins-A, surfactant proteins-B, surfactant proteins-C, and surfactant proteins-D. Clinical, epidemiological, and biochemical evidence suggests that the etiology of respiratory distress syndrome is multifactorial with a significant genetic component. There are reports about polymorphisms and mutations on the surfactant protein genes, especially surfactant proteins-B, that may be associated with respiratory distress syndrome, acute respiratory distress syndrome, and congenital alveolar proteinosis. Individual differences regarding respiratory distress syndrome and acute respiratory distress syndrome as well as patient response to therapy might reflect phenotypic diversity due to genetic variation, in part. The study of the differences between the allelic variants of the surfactant protein genes can contribute to the understanding of individual susceptibility to the development of several pulmonary diseases. The identification of the polymorphisms and mutations that are indeed important for the pathogenesis of the diseases related to surfactant protein dysfunction, leading to the possibility of genotyping individuals at increased risk, constitutes a new research field. In the future, findings in these endeavors may enable more effective genetic counseling as well as the development of prophylactic and therapeutic strategies that would provide a real impact on the management of newborns with respiratory distress syndrome and other pulmonary diseases.


O surfactante pulmonar é uma substância composta por um complexo lipoprotéico essencial para a função pulmonar normal. As proteínas do surfactante têm importante papel na estrutura, função e metabolismo do surfactante. São descritas quatro proteínas específicas denominadas surfactante pulmonar-A, surfactante pulmonar-B, surfactante pulmonar-C e surfactante pulmonar-D. Evidências clínicas, epidemiológicas e bioquímicas sugerem que a etiologia da síndrome do desconforto respiratório é multifatorial com um componente genético significativo. Existem na literatura algumas descrições sobre a presença de polimorfismos e mutações em genes dos componentes do surfactante, particularmente no gene da surfactante pulmonar-B, os quais parecem estar associados à síndrome do desconforto respiratório, síndrome da angustia respiratória aguda e proteinose alveolar congênita. Diferenças individuais relacionadas à síndrome do desconforto respiratórioe síndrome da angustia respiratória aguda e à resposta dos pacientes ao tratamento podem refletir diversidade fenotípica, devido, parcialmente, à variação genética. O estudo das diferenças entre as variantes alélicas dos genes das proteínas do surfactante pode ajudar na compreensão das variabilidades individuais na susceptibilidade ao desenvolvimento de várias doenças pulmonares. A determinação de quais polimorfismos e mutações são, de fato, importantes na patogênese das doenças relacionadas à disfunção das proteínas do surfactante e a possibilidade da realização da genotipagem em indivíduos de alto risco constitui um novo campo de pesquisa, que pode permitir, futuramente, um aconselhamento genético mais efetivo, resultando no desenvolvimento de estratégias profiláticas e terapêuticas que representem um impacto real no manejo dos recém-nascidos portadores da síndrome do desconforto respiratório e outras patologias pulmonares.


Subject(s)
Humans , Infant, Newborn , Mutation , Pulmonary Surfactant-Associated Proteins/genetics , Pulmonary Surfactants/metabolism , Respiratory Distress Syndrome, Newborn/genetics , Genetic Predisposition to Disease , Genetic Variation , Polymorphism, Genetic , Pulmonary Alveolar Proteinosis/genetics , Pulmonary Alveolar Proteinosis/metabolism , Pulmonary Surfactant-Associated Protein A/deficiency , Pulmonary Surfactant-Associated Protein B/deficiency , Pulmonary Surfactant-Associated Protein C/deficiency , Pulmonary Surfactant-Associated Protein D/deficiency , Pulmonary Surfactant-Associated Proteins/metabolism , Respiratory Distress Syndrome, Newborn/metabolism
11.
Article in Chinese | WPRIM | ID: wpr-813951

ABSTRACT

OBJECTIVE@#To explore the effect of hepatocyte growth factor (HGF) on the proliferation, apoptosis and function of hyperoxia exposed Type II alveolar epithelial cells (AEC II) isolated from premature rat lungs, and to explore the mechanism of the protective effect of HGF on hyperoxia-induced lung injury.@*METHODS@#Type II alveolar epithelial cells from fetal rat lungs were cultured. After being purified, AEC II was randomly divided to 4 groups: air group (Air), hyperoxia group (HO), air plus hepatocyte growth factor group (Air+HGF), hyperoxia plus hepatocyte growth factor group (HO+HGF) . The mRNA levels of surfactant associated protein, SPs (including SPA, SPB, SPC) were measured by RT-PCR. The proliferation and apoptosis of AEC II were analyzed with flow cytometric assay and Western blot.@*RESULTS@#(1) Compared with Air group, the apoptosis rate increased significantly in the HO group, while G(2)/M phase percentage and the protein expression levels of proliferating cell nuclear antigen (PCNA) decreased significantly (P<0.01); the S phase percentage and the protein expression levels of PCNA increased significantly in the Air+HGF group. (2) In the HO +HGF group, the apoptosis rate was not significantly different, G0/G1 phase percentage decreased significantly, S phase, G(2)/M phase percentage and the protein expression levels of PCNA increased significantly compared with the HO group. (3) SPs mRNA levels significantly decreased in the HO group compared with those in the Air group. After HGF was added, SPs mRNA levels increased in the HO +HGF group and the Air+HGF group compared with the HO group.@*CONCLUSION@#Hyperoxia can inhibit the proliferation, increase the apoptosis rate and decrease SPs mRNAs levels of AEC II in vitro in premature rats, while HGF can partly inhibit the changes of SPs mRNAs levels and cell proliferation of AEC II resulted from hyperoxia, and HGF may play a protective role in hyperoxia-induced lung injury.


Subject(s)
Animals , Animals, Newborn , Apoptosis , Cell Proliferation , Cells, Cultured , Epithelial Cells , Metabolism , Female , Hepatocyte Growth Factor , Pharmacology , Hyperoxia , Metabolism , Pathology , Male , Pregnancy , Proliferating Cell Nuclear Antigen , Metabolism , Pulmonary Alveoli , Cell Biology , Pulmonary Surfactant-Associated Proteins , Metabolism , Rats , Rats, Sprague-Dawley
12.
Article in English | WPRIM | ID: wpr-24297

ABSTRACT

BACKGROUND: Pulmonary damage resulting from lipid peroxidation is a principal effect of paraquat intoxication. The host-defense functions of surfactant are known to be mediated by the surfactant proteins A and D (SP-A and SP-D, respectively). The primary objective of this study was to evaluate the variations over time in levels of surfactant protein and lipid peroxidation (LPO) in lung tissue following free-radical-induced injury. METHODS: 42 adult, male, Sprague-Dawley rats were administered intraperitoneal injections of paraquat (35 mg/kg body weight). SP-A and SP-D levels were determined via Western blot. LPO in the left lung homogenate was measured via analyses of the levels of thiobarbituric acid-reactive substances. RESULTS: LPO levels peaked at 6 hours, with no associated histological changes. SP-D levels increased until hour 12 and declined until hour 48; SP-D levels subsequently began to increase again, peaking at hour 72. SP-A levels peaked at hour 6, declining thereafter. CONCLUSIONS: We suggest that in the early phase of paraquat injury, SP-D levels reflect alveolar damage and that de novo synthesis of SP-D takes 72 hours. Levels of SP-A, on the other hand, reflect abnormalities in the surfactant system in the late stage of paraquat intoxication. Surfactant proteins may play a role in protecting the lungs from reactive oxygen injury. A time-dependent variation has been observed in the levels of surfactant proteins A and D following paraquat injury, and it has been suggested that these proteins play a role in the protection of lung tissue against ROS-induced injuries.


Subject(s)
Animals , Free Radicals/toxicity , Herbicides/toxicity , Lipid Peroxidation , Lung/drug effects , Male , Paraquat/toxicity , Pulmonary Surfactant-Associated Proteins/analysis , Rats , Rats, Sprague-Dawley , Reactive Oxygen Species/toxicity , Respiratory Distress Syndrome/chemically induced
13.
Article in Vietnamese | WPRIM | ID: wpr-578

ABSTRACT

Background: Respiratory distress is one among the leading reasons cause mortality for infants especially for preterm babies or light weight babies. Surfactant therapy in premature infants can decrease mortality, duration of respiratory treatment, pulmonary air leaks and chronic lung disease. Objective: This study aims to assess the effect of surfactant therapy in premature infants with respiratory distress syndrome at Intensive Care Unit of Children Hospital N\xb0.2. Subjects and method:A cases study about premature infants less than 24 hours after birth with respiratory distress syndrome (RDS) admitted to intensive care unit and treated with surfactant from January 2007 to July 2007 at the Children Hospital No 2. There were 30 cases recruited. The data was collected and analyzed by EpiInfo software 2002.Results: Most of them improved in respiration status after using surfactant (96.7%); no case of air leak was seen; 3 bronchopulmonary dysplasia cases and 4 deaths due to nosocomial infection were seen. Conclusion: Surfactant therapy was effective in premature infants with RDS. In the case of having economic advantages, surfactant may be indicated for preventive treatment on the premature and light weigh infants without respiratory distress syndrome on clinical aspect.


Subject(s)
Respiratory Distress Syndrome, Newborn , Infant, Newborn , Pulmonary Surfactant-Associated Proteins , Infant
14.
Clinics ; 61(2): 153-160, Apr. 2006. graf
Article in English | LILACS, SES-SP | ID: lil-426297

ABSTRACT

OBJETIVO: Estudar a imunogenicidade e a estabilidade do surfactante de origem porcina produzido pelo Instituto Butantan. MÉTODO: Experimento imunogenicidade: 16 coelhos da raça New-Zealand-White (Peso de 1000g) foram divididos em grupos de 4 animais. Cada grupo foi designado para receber: a) Surfactante do Butantan, b) Survanta® (Abbott Laboratories), c) Curosurf (Farmalab Chiesi) e d) nenhum tratamento com surfactante. Os surfactantes foram administrados via intratraqueal e o sangue dos animais foi coletado antes, 60 e 180 dias após a administração do surfactante. O soro obtido foi analisado quanto a presença de anticorpos anti-surfactante pelo método ELISA (enzyme-linked immunosorbent assay). Experimento estabilidade: O surfactante do Butantan usado neste experimento tinha sido armazenado por um ano em refrigerador (4 a 8°C) e sua estabilidade foi analisada em condições distintas de experimentação, usando o modelo de coelho prematuro. RESULTADOS: Experimento imunogenicidade: Nenhum dos surfactantes analisados determinou a produção de anticorpos contra seus constituintes. Experimento estabilidade: Os resultados deste estudo demonstraram que o surfactante do Instituto Butantan mostrou eficácia semelhante a do Curosurf após ter sido submetido à condições adversas ao longo do tempo. A eficácia foi demonstrada através da complacência pulmonar dinâmica, pressão ventilatória e da curva pressão-volume. CONCLUSÃO: Os resultados deste estudo demonstraram que o surfactante do Instituto Butantan pode representar um tratamento alternativo de reposição de surfactante.


Subject(s)
Animals , Female , Pregnancy , Rabbits , Pulmonary Surfactants/chemistry , Pulmonary Surfactants/immunology , Models, Animal , Animals, Newborn , Respiratory Tract Diseases/drug therapy , Time Factors , Pulmonary Surfactant-Associated Proteins/immunology , Pulmonary Surfactants/therapeutic use , Swine
15.
Chinese Journal of Pediatrics ; (12): 450-453, 2004.
Article in Chinese | WPRIM | ID: wpr-340305

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effects of maternally administered dexamethasone and ambroxol on the mRNA levels of surfactant proteins (SP-A, SP-B and SP-C) expression in fetal rat lungs at gestational age day 19.</p><p><b>METHODS</b>A 19-day fetal rat lung model was employed. In situ hybridization was used to detect the expression of SP-B mRNA in alveolar type II cell, and the levels of SP-A, SP-B and SP-C mRNAs were detected by semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>(1) SP-B mRNA was detected in situ in alveolar type II cells in fetal rat lung of day 19 gestational age; (2) In the late developmental period of fetal rat lungs, alveolar type II cells were also found around bronchus; (3) Comparing to beta-actin mRNA, the relative values of SP-A, SP-B and SP-C mRNAs were 0.81 +/- 0.26, 0.97 +/- 0.20 and 0.88 +/- 0.11 in fetal lung in the control group. The relative values of mRNAs of SP-A, SP-B and SP-C to beta-actin were 1.04 +/- 0.16, 1.28 +/- 0.29, 1.09 +/- 0.25 in fetal lungs of the ambroxol injected rats, and were 1.08 +/- 0.25, 1.23 +/- 0.35, 1.21 +/- 0.25 in fetal lungs of the dexamethasone injected rats, respectively. Both ambroxol and dexamethasone-treated rats had significantly higher mRNA expression of surfactant proteins compared to the control saline injected animals (P < 0.05). (4) There were no significant differences between ambroxol and dexamethasone in the effects of increasing expressions of surfactant protein mRNAs (P > 0.05).</p><p><b>CONCLUSION</b>Antepartum administration of both ambroxol and dexamethasone can significantly increase fetal lung SP-A, SP-B and SP-C mRNAs expression.</p>


Subject(s)
Ambroxol , Pharmacology , Animals , Dexamethasone , Pharmacology , Expectorants , Pharmacology , Female , Gene Expression Regulation, Developmental , Glucocorticoids , Pharmacology , Lung , Embryology , Metabolism , Pregnancy , Pulmonary Surfactant-Associated Protein A , Genetics , Pulmonary Surfactant-Associated Protein B , Genetics , Pulmonary Surfactant-Associated Protein C , Genetics , Pulmonary Surfactant-Associated Proteins , Genetics , RNA, Messenger , Genetics , Metabolism , Rats , Rats, Wistar , Reverse Transcriptase Polymerase Chain Reaction
16.
Salud(i)ciencia (Impresa) ; 11(5): 21-23, 2003. graf., tab.
Article in Spanish | LILACS | ID: biblio-1377822

ABSTRACT

Los análisis de regresión identificaron variantes genéticas de proteínas surfactantes o alelos asociados con aumento o disminución del riesgo (susceptibilidad), lo que sugiere que las variantes genéticas son marcadores útiles para el estudio de la tuberculosis.


Subject(s)
Tuberculosis , Proteins , Surface-Active Agents , Risk , Regression Analysis , Pulmonary Surfactant-Associated Proteins , Disease Susceptibility , Alleles
17.
Article in Chinese | WPRIM | ID: wpr-339659

ABSTRACT

<p><b>AIM</b>To investigate the effects of ischemic preconditioning on reperfusion injury of rat lung.</p><p><b>METHODS</b>Rat isolated lungs (n=8 in each group) were stabilized and perfused by Krebs-Henseleit solution on a modified langendorff perfusion apparatus. 36 wistar rats were divided into three groups: ischemic preconditioning group, ischemia/reperfusion group and control group. Mean pulmonary artery pressure, wet/dry ratio, pulmonary surfactant phospholipid and alveolar surface tension in bronchoalveolar lavage fluid and electron microscope were detected.</p><p><b>RESULTS</b>The morphological changes of lung injury were alleviated in the preconditioning group under electron microscope. Wet/dry ratio, mean pulmonary artery pressure and SA/LA ratio were significantly lower in the preconditioning group after ischemic/reperfusion (P < 0.01). Total phospholipid and large aggregate in the BALF were significantly increased in the preconditioning group (P < 0.01). Small aggregate showed no change in three groups. Surfactant activity test showed that surface tension markedly decreased in IPC group (P < 0.01).</p><p><b>CONCLUSION</b>These results indicates that ischemic preconditioning may have a protective effect in ischemic/reperfusion injuries lung by ameliorating the content and function of surfactant phospholipid.</p>


Subject(s)
Animals , Ischemic Preconditioning , Methods , Lung , Metabolism , Pathology , Pulmonary Surfactant-Associated Proteins , Bodily Secretions , Rats , Rats, Wistar , Reperfusion Injury
18.
Article in English | WPRIM | ID: wpr-38940

ABSTRACT

BACKGROUND: All organisms have developed an internal timing system capable of reacting to and anticipating environmental stimuli with a program of appropriately timed metabolic, physiologic and behavioral events. The alveolar epithelial type II cell of the mammalian lung synthesizes, stores, and secretes a lipoprotein pulmonary surfactant, which functions to stabilize alveoli at low lung volumes. METHODS: The authors investigated the diurnal variation of surfactant protein A, B and C mRNA accumulation. The diurnal variation on gene expression of surfactant protein A, B and C was analysed using filter hybridization at 9 a.m., 4 p.m. and 11 p.m. Lung SP-A protein content was determined by double sandwich ELISA assay using a polyclonal antiserum raised in rabbits against purified rat SP-A. RESULTS: 1. The accumulation of SP-A mRNA at 4 p.m. was significantly decreased by 23.5% compared to the value at 9 a.m. (p< 0.05). 2. The accumulation of SP-B mRNA at 4 p.m. and 11 p.m. was decreased by 15.1% and 5.7%, respectively, compared to the value at 9 a.m. (p=0.07, p=0.69). 3. The accumulation of SP-C mRNA at 4 p.m. and 11 p.m. was decreased by 6.8% and 7.7%, respectively, compared to the value at 9 a.m. (p=0.38, p=0.57). 4. Total lung SP-A content at 4 p.m. and 11 p.m. was increased by 5.3% and 15.9%, respectively, compared to the value at 9 a.m. (p=0.64, p=0.47). CONCLUSION: These findings represent the diurnal variation of surfactant proteins mRNA expression in vivo. These results indicated that the diurnal variation of significant gene expression is observed in hydrophilic surfactant protein rather than in hydrophobic surfactant proteins.


Subject(s)
Animals , Circadian Rhythm , Enzyme-Linked Immunosorbent Assay , Gene Expression , Pulmonary Surfactant-Associated Proteins/genetics , RNA, Messenger/metabolism , Rats , Rats, Sprague-Dawley
19.
Chinese Medical Journal ; (24): 1099-1100, 2002.
Article in English | WPRIM | ID: wpr-340375

ABSTRACT

Pulmonary surfactant ( PS ) compromises lipids and surfactant proteins (SP) and lines on the alveolar air-liquid interface. It can reduce surface tension, prevent alveoli from collapse and reduce alveoli edema by disaturated dipalmitoylphosphatidylcholine. It also modulates the pulmonary immunology by SP-A and SP-D. In this study,we established a rat model of immunocompromised host (ICH) with pulmonary infection of Pseudomonas aeruginosa (P. aeruginosa), then studied its pulmonary inflammatory reaction and analyzed the concentration of lipids and SP-A in bronchoalveolar lavage fluid (BALF) during infection.


Subject(s)
Animals , Bronchoalveolar Lavage Fluid , Chemistry , Microbiology , Lipids , Lung , Microbiology , Male , Neutrophils , Physiology , Pneumonia, Bacterial , Allergy and Immunology , Metabolism , Proteolipids , Pseudomonas Infections , Allergy and Immunology , Metabolism , Pulmonary Surfactant-Associated Protein A , Pulmonary Surfactant-Associated Proteins , Pulmonary Surfactants , Rats , Rats, Sprague-Dawley
20.
Indian J Pediatr ; 1998 Nov-Dec; 65(6): 781-95
Article in English | IMSEAR | ID: sea-79987

ABSTRACT

Pulmonary surfactant is a lipoprotein substance that lines the lungs and helps reduce surface tension. Surfactant associated protein-A (SP-A) is the most abundant non-serum protein in pulmonary surfactant. This complex glycoprotein aids in the synthesis, secretion and recycling of surfactant phospholipids, and facilitates the reduction of surface tension by surfactant phospholipids. Recent evidence has highlighted the role of SP-A in the innate immune system present in the lung. SP-A may play a major role in defense against pathogens by interacting with both infectious agents and the immune system. Factors that affect fetal lung maturation, e.g. gestational age and hormones regulate SP-A gene expression. Mediators of immune function also regulate SP-A levels. A number of lung disorders, including infectious diseases and respiratory distress syndrome are associated with abnormal alveolar SP-A levels. SP-A can no longer be called a lung-specific protein, since it has recently been detected in other tissues. In most species, SP-A is encoded by a single gene, however in humans it is encoded by two, very similar genes. Models for the structure of the human SP-A protein molecule have been proposed, suggesting that the mature alveolar SP-A molecule is composed of both gene products. The study of SP-A may provide information helpful in understanding disease processes and formulating new treatment modalities.


Subject(s)
Gene Expression/physiology , Humans , Infant , Infant, Newborn , Organ Specificity , Proteolipids/genetics , Pulmonary Alveoli/physiopathology , Pulmonary Surfactant-Associated Protein A , Pulmonary Surfactant-Associated Proteins , Pulmonary Surfactants/genetics , Respiratory Distress Syndrome, Newborn/physiopathology , Respiratory Tract Infections/physiopathology , Surface Tension
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