Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Adicionar filtros








Intervalo de ano
1.
Chongqing Medicine ; (36): 151-154, 2015.
Artigo em Chinês | WPRIM | ID: wpr-462828

RESUMO

Objective To investigate the effect of IL‐1βon the expression and release of high mobility group box 1 (HMGB1) from normal human bronchiolar epithelial cell (HBE) .Methods HBE135‐E6E7 was developed and methyltetrazolium (MTT) as‐say was used to assess the viability of HBE cell line under different concentration of IL‐1β.The mRNA expression of HMGB1 in HBE after stimulating with IL‐1βwere determined by Real‐time PCR;the level and location of HMGB1 in the cytoplasm ,nucleus and culture medium of HBE after stimulating with IL‐1β were detected by Western blot and ELISA assay .The expression and translocation of HMGB1 of HBE after stimulating with IL‐1β were detected by Immunofluorescence .Results 0 .1 ,1 .0 ,10 .0 ng/mL IL‐1βdid not influence the cell viability of HBE ;IL‐1β increased the mRNA expression of HMGB1 in HBE in does‐and time‐dependent manner and increased the protein expression of HMGB1 in HBE .In comparison with control group ,the levels of HMGB1 in the culture medium significantly increased after stimulation with IL‐1βat 1 .0 ,10 .0 ng/mL for 24 h(P<0 .05)in the dose dependent experiments;and in time dependent experiments ,10 .0 ng/mL IL‐1βsignificantly increased HMGB1 level in the cul‐ture medium after stimulation for both 12 h and 24 h (P< 0 .05) .After stimulation with IL‐1β (10 .0 ng/mL ) for 24 h ,the HMGB1 expression in cytoplasm significantly increased in plasmosin and decreased in nucleus .HMGB1 translocated from nuclei to cytoplasm after stimulation with IL‐1β(10 .0 ng/mL ) for 24 h .Conclusion IL‐1βcould induce HMGB1 expression and release in human bronchial epithelial cells ,which indicates that HMGB1 may involve in IL‐1β‐mediated chronic airway inflammation .

2.
The Journal of Practical Medicine ; (24): 2591-2594, 2014.
Artigo em Chinês | WPRIM | ID: wpr-455208

RESUMO

Objective To detect the pre- and post-treatment levels of serum interleukin (IL-20) in asthmatic patients during the acute exacerbation period and to investigate the role of IL-20 in the pathogenesis of bronchial asthma and relative clinical significance. Methods Forty-five cases of mild to moderate asthma outpatients in the First Affiliated Hospital of Guangxi Medical University from May 2013 to October 2013 were chosen as the asthma group and 32 healthy people who underwent routine physical examination as the control group. All the patients were treated with inhalation salmeterol and fluticasone 50/250 μg/μg (sucking twice a day) together with ventolin if necessary , and even with theophylline sustained-release tablets as the additional treatment in moderate asthma group for 1 week. The serum levels of IL-20 as well as immunoglobulin E (IgE) were detected by ELISA in the asthma group before and after treatment as well as in the control group. Other data including ECP , the number of eosinophil ceils (EOS) and the pulmonary function (FEV1%) were detected as well. The differences of IL-20 levels between the asthma group before and after treatment and the control group were analyzed and the correlation between IL-20 and Ig E, EOS, ECP and FEV1% were analyzed. Results Compared with the healthy control group [(13.58 ± 6.17)pg/L], the levels of IL-20 in the mild and moderate asthma pretreatment group were significantly increased [(23.43 ± 13.60)pg/L and (33.78 ± 22.69)pg/L]. Compared with the mild asthma group, the levels of IL-20 in the moderate asthma pretreatment group were significantly higher. After treatment , the levels of IL-20 [(15.73 ± 8.27)pg/L and (19.64 ± 11.69)pg/L] were decreased respectively in the asthmatic patients. The Pearson correlative analysis showed that there were positive correlations between the levels of 1L-20 and IgE , EOS and ECP respectively and there were negative correlations between IL-20 levels and FEV1%. Conclusion IL-20 may be involved in the pathogenesis of asthma.

SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA