ABSTRACT
OBJECTIVE: To observe the effect of Benzamil on cytosolic free calcium ions ([Ca(2+)] i) concentration, tumor necrosis factor-alpha (TNF-alpha) and malondialdehyde (MDA) in alveolar macrophage (AM) in patients with chronic obstructive pulmonary disease (COPD). METHODS: Alveolar macrophages were collected from bronchoalveolar lavage fluid, and they were cultured and [Ca(2+)] i were determined by calcium fluorescent with indicator Fura-2/AM. The effects of Benzamil on the increase in cytosolic [Ca(2+)] i and on secretion of TNF-alpha, MDA were investigated in 36 patients with COPD and 36 healthy volunteers. RESULTS: (1) [Ca(2+)] i concentration (68.26+/-7.24) nmol/L, TNF-alpha (5.74+/-0.42) ng/L and MDA (3.77+/-0.61) microg/L were found in COPD patients, and they were significantly increased, as compared with the control group, in whom the contents were [Ca(2+)] i concentration (60.61+/-6.26) nmol/L, TNF-alpha (2.06+/-0.20) microg/L, MDA (1.91+/-0.19) ng/L (all P<0.01). (2)The following data namely [Ca(2+)] i concentration (168.34+/-17.58) nmol/L, TNF-alpha (9.67+/-1.01) ng/L and MDA (11.21+/-1.01) microg/L were obtained after anoxia in COPD patients (all P<0.01). (3)After incubation with Benzamil, and then subjected the cells to anoxia, the following data were obtained: [Ca(2+)] i concentration (129.21+/-14.33) nmol/L, TNF-alpha content (6.78+/-0.52) ng/L and MDA (8.47+/-0.79) microg/L and they were all lower than only anoxia was applied (all P<0.01). CONCLUSION: Benzamil not only downregulates alveolar macrophages activity but also suppresses the generation of the TNF-alpha and MDA.
Subject(s)
Amiloride/analogs & derivatives , Macrophages, Alveolar/metabolism , Pulmonary Disease, Chronic Obstructive/metabolism , Sodium-Calcium Exchanger/antagonists & inhibitors , Aged , Amiloride/pharmacology , Bronchoalveolar Lavage Fluid/cytology , Calcium/metabolism , Cells, Cultured , Female , Humans , Macrophages, Alveolar/drug effects , Male , Malondialdehyde/metabolism , Middle Aged , Pulmonary Disease, Chronic Obstructive/pathology , Tumor Necrosis Factor-alpha/metabolismABSTRACT
OBJECTIVE: To explore the effects of bilirubin on expression of laminin (Ln) and epidermal growth factor (EGF) in lung tissue and in type II pneumocytes (ATII) in smoking rats. METHODS: 36 healthy Wistar rats were randomly divided into three groups: a normal group, a smoking-induced emphysema model group (model group), and a bilirubin group (n = 12, for each group). According to XU San-lin method, rats both in the model group and the bilirubin group were exposed to smoke for a total of 6 months. Rats in the bilirubin group were pretreated with indirect bilirubin (20 mg.kg(-1).d(-1)) before exposed to smoke once a day. All animals were sacrificed six months later. ATIIwere isolated, purified and cultured. Ln in ATII culture medium was determined by radioimmunoassay (RIA). We detected Ln in lung tissue with indirect immunofluorescence technique and EGF with immunochemistry. RESULTS: In the model group, Ln content in ATII culture medium and in lung tissue [(5.0 +/- 0.3) mg/ml, 5.67 +/- 0.26] increased significantly compared with those in the normal group [(3.2 +/- 0.5) mg/ml, 2.01 +/- 0.74; P < 0.05, respectively]. In the bilirubin group, the two indexes [(3.9 +/- 0.7) mg/ml, 4.18 +/- 0.63] decreased significantly compared with those in the model group (P < 0.05, respectively), which was higher than the normal group (P < 0.05). Expression of EGF in lung tissue of the model group (0.43 +/- 0.09) increased significantly compared with that of the normal group (0.14 +/- 0.02; P < 0.05). The expression of EGF in the bilirubin group (0.34 +/- 0.03) decreased significantly compared with the model group (P < 0.05), which was higher than that of the normal group. CONCLUSIONS: Bilirubin was shown to be able to promote the reconstruction of extracellular matrix by decreasing the expression of Ln and EGF in lung tissue and in ATII in the development of emphysema.
Subject(s)
Bilirubin/pharmacology , Epidermal Growth Factor/metabolism , Laminin/metabolism , Pulmonary Emphysema/metabolism , Smoking/adverse effects , Animals , Cells, Cultured , Female , Lung/metabolism , Lung/pathology , Male , Pulmonary Alveoli/metabolism , Pulmonary Alveoli/pathology , Pulmonary Emphysema/etiology , Pulmonary Emphysema/pathology , Random Allocation , Rats , Rats, WistarABSTRACT
OBJECTIVE: To obtain the epidemiological data of sleep apnea-hypopnea sydrome (SAHS) in Taiyuan. METHODS: A questionnaire survey was performed in 6 028 people living in Taiyuan. The prevalence of SAHS was estimated by a two-stage procedure. In the first stage, stratified cluster disproportional random sampling survey was performed in Taiyuan. 6 028 questionnaires were send to random sample of defined population in the 4 sites selected from 2 districts. The response rate was 85.11%. During the second stage 476 of those highly suspected of having SAHS (ESS >/= 9) underwent all-night polysomnographic (PSG) studies. RESULTS: From the study population, 179 were diagnosed as having SAHS. The overall prevalence was 3.5% (male 4.7% and female 1.9%). CONCLUSION: The prevalence of SAHS was 3.5% among Taiyuan.
