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Objective To analyze the change in the concentration of IL-17 and IL-10 inflammatory factors among the deadaptation personnel who returned from the plateau.Methods A total 21 healthy males were investigated who averaged 25 years in age, lived permanently in the plains (200 m), and once stayed to the plateau (Lasha) for 6 months.Their venous blood was collected at three time points:the day before ascending to the plateau(control), the second day after return to the plains(d2) and the 30th day(d30), respectively.Their serum was seperated from the whole blood and the level of IL-17A and IL-10 was detected by ELISA method.Results The concentration of IL-17A and the IL-17A/IL-10 ratio were significant increased at d2 and d30, respectively, compared with control (P<0.05).Compared with d2, IL-17A and the IL-17A/IL-10 ratio were decreased obviously at d30(P <0.05).The level of IL-10 at d2 and d30 was significantly reduced compared with control ( P <0.05), but increased at d30 compared with d2.Correlative analysis showed that there was a negative correlation in the levels of IL-10 and IL-17A between control, d2 and d30, respectively (r1=0.948, P<0.05;r2=0.969, P<0.05;r3=0.972, P<0.05).A significant negative correlation was observed in the alteration levels of IL-10 and IL-17A between the three groups(r4=-0.793, P<0.05; r5=-0.756, P<0.05). Conclusion The concentration of inflammatory factors among the plateau deadaptation patients is imbalanced, but it is gradually reduced with time.The mechanism is still not clear.
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Objective To construct the bait plasmid of pSos-single immunoglobin IL-1 receptor related protein (SIGIRR) in Cy-toTrap yeast two hybrid system ,and to test its self-activation .Methods The cDNA fragments of SIGIRR(480 -1 230 bp) were amplified from pReceiver-LV19-SIGIRR and ligated into the bait plasmid pSos to generate the plasmid pSos-SIGIRR .The pSos-SI-GIRR was identified by DNA sequencing and dual-site endonuclease digestion .Then the recombinant plasmid and control plasmid were introduced into the yeast cell cdc25H .The transformants were inoculated on plates of 25 ℃ /SD/Glucose(-UL) ,25 ℃/SD/Ga-lactose(-UL) ,37 ℃ /SD/Glucose(-UL) and 37 ℃ /SD/Galactose ,respectively and the proliferation ability of transformant was ob-served for 6 d .The Western blot was adopted to detect the expression of target protein .Results The pSos-SIGIRR vector was cor-rectly constructed and proved of no self-activation and toxic action .The Western blot showed that the target protein was expressed in a form of fusion protein of 170KD .Conclusion The bait plasmid containing SIGIRR cytoplasmic tail can be applied to the yeast two-hybrid system and lays the important foundation for seeking the interacting protein with SIGRR from the human lung cDNA li-brary in .
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Objective To observe the proliferation and phenotype-switching of pulmonary arterial smooth muscle cell (PASMC) induced by hypoxia and interfered by Ad-PKGIα. And to investigate the potential regulative role of PKGIα gene in the molecule mechanism of hypoxia pulmonary vessel remodeling (HPVR). Methods To establish the pure PASMC cultured by tissue-sticking methods. Semi-quantitative reverse transcription and polymerase chain reaction (RT-PCR) and Western blot were used to examine the PKGIα mRNA and protein expression after PASMC were transfected by Ad-PKG. The mRNA and protein expressive change of smooth muscle α actin(SM-α-actin) determined the degree of cell phenotype-switching. The changes of PASMC proliferation were determined by flow cytometry and ~3H-TdR incorporated way. Results Ad-PKGIα could transfect into PASMC and highly express. Hypoxia down-regulated the expression of SM-α-actin protein (44. 25±5.34 in normoxia, 32. 18±4. 19 in 12 h hypoxia condition, 21.90 ±2. 44 in 24 h hypoxia condition, P < 0. 05), that could be blocked by the transfeetion of Ad-PKGIα. Hypoxia could push PASMC mitosis and proliferating(~3H-TdR incorporated way: 7570 ± 371 in normoxia,12 020± 831 in 12 h hypoxia condition,14 924 ± 1491 in 24 h hypoxia condition, P <0. 05), that could be blocked by the transfection of Ad-PKGIα, too. Conclusions The results suggested that PKGIα signaling pathway might play an important role in the molecule mechanism of HPVR. And PKGIα gene might be a target point of gene therapy.
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Gax gene is a newly found negative transcriptional regulator of cells proliferation. This paper introduces the detection and structural features of Gax, details the inhibitory effect of Gax on the proliferation of vascular smooth muscle cells, vascular endothelial cells and cancer cells, and explains the putative mechanisms therein involved. The potential for providing therapeutic insights into human diseases by modulating Gax activity is prospected.
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Humans , Cell Proliferation , Cells, Cultured , Endothelial Cells , Cell Biology , Gene Expression , Homeodomain Proteins , Genetics , Metabolism , Muscle, Smooth, Vascular , Cell BiologyABSTRACT
BACKGROUND: Dendritic cells, the most potent antigen presenting cells known at present, have been extensively used in the immunotherapy as adjuvant. OBJECTIVE: The present study was to construct Der p 2 eukaryotic expression vector and validate its expression in the mouse bone marrow-derived dendritic cells. DESIGN, TIME AND SETTING: A single sample observation was performed at the Institute of Respiratory Disease,Xinqiao Hospital, Third Military Medical University of Chinese PLA between May and December 2005. MATERIALS: C57BL/6 mice were included. Plambd-Der p 2 was the product of Heska Company, USA.pCI-neo plasmid was provided by the Institute of Respiratory Disease, Xinqiao Hospital, Third Military Medical University of Chinese PLA.METHODS: Mouse bone marrow-derived dendritic cells were in vitro isolated and cultured.Complete Der p 2 cDNA was spliced from prokaryotic expression vector plambd-Der p 2, and then cloned into eukaryotic expression vector pCI-neo (pCI-neo-Der p 2).The positive recombinants pCl-neo-Der p 2 transfected into dendritic cells.Non-transfected and blank vector pCI-neo-transfected dendritic cells were used as controls. MAIN OUTCOME MEASURES: ①Identification of pCI-neo-Der p 2 recombinant plasmid.②Detection of Der p 2 mRNA and protein expression by reverse transcription-polymerase chain reaction (RT-PCR) and Western Blot techniques. RESULTS: Sequencing results showed Der p 2 cDNA in pCI-neo-Der p 2 was in coincidence with the sequence registrated in Gene Bank.RT-PCR and Western Blot results showed that expression of Der p 2 mRNA and protein could be detectable in the pCI-neo-Der p 2-transfected dendritic cells. CONCLUSION: The Der p 2 cDNA was successfully constructed into the eukaryotic expression vector, and Der p 2 gene and protein could be expressed efficiently in dendritic cells.
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<p><b>BACKGROUND</b>Apoptosis is closely related to development of lung cancer. It is a strategy of lung cancer therapy to induce apoptosis. The aim of this study is to explore the effects of growth arrest-specific homeobox (Gax) transfection on apoptosis and expression of Bcl-2 and Bax proteins of human lung adenocarcinoma A549 cells.</p><p><b>METHODS</b>A549 cells were transfected with Gax gene by a replication-deficient adenovirus expressing the hemagglutinin-tagged Gax cDNA (Ad-Gax). Apoptosis of A549 cells was observed by transmission electronic microscope and terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) positive staining. Apoptotic rate of A549 cells was evaluated by flow cytometry. Expressions of Bcl-2 and Bax proteins in A549 cells were detected by immunocytochemistry.</p><p><b>RESULTS</b>Before Ad-Gax transfection, none or few of TUNEL-positive A549 cells were detected. After Ad-Gax transfection, a marked increase in TUNEL-positive staining occurred, especially at 24 h later. The ratio of apoptosis of A549 cellsin non-transfection group and transfection groups at 12 h, 24 h, 48 h were 0.25%, 12.57%, 17.29%, 15.03%, respectively. Compared with non-transfection group, the apoptotic rates of transfection groups increased significantly (Chi-square value was 7.357, 11.126 and 9.943 respectively, P < 0.01). The average optical density (AOD) of Bcl-2 protein in A549 cells in non-transfection group and transfection groups at 12 h, 24 h, 48 h were 2.02±0.07, 1.79±0.02, 1.25±0.51 and 1.21±0.24 respectively. Compared with non-transfection group, AOD of Bcl-2 protein in A549 cells in transfection groups decreased significantly (t value was 6.651, 7.089 and 7.438 respectively, P < 0.01). On the other hand, Bax protein expression in transfection groups increased, the AODs of Bax were 4.49±0.61, 4.24±0.37 and 3.95±0.43, respectively. Compared with non-transfection group (3.12±0.42), AOD of Bax protein in A549 celle in transfection groups increased significantly (t value was 7.469, 7.287 and 6.473 respectively, P < 0.01). In the Ad-Gax transfection groups the lower Bcl-2/Bax ratio was, the higher the apoptotic rate of A549 cells was (r=-0.49, P < 0.01).</p><p><b>CONCLUSIONS</b>Ad-Gax transfection can induce A549 cells apoptosis. Possible mechanism is that Gax can downregulate Bcl-2 protein expression and upregulate Bax protein expression, and A549 cells apoptosis is related to the Bcl-2/Bax ratio.</p>
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The number of taking the Examination of Doctor Qualification is rising,while the pass rate is dropping each year.This status has undoubtedly made a big challenge for clinical teaching,and how to improve the effects of clinical lessons has become an important topic for the clinical teachers.The Affiliated Xinqiao Hospital of the Third Military Medical University has made some new changes in clinical teaching mode,which has a study clue of organ and system.Those methods give much help for students to pass the Examination of Doctor Qualification.
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<p><b>BACKGROUND</b>Lung cancer is the leading cancer of malignant tumor in China.It is the direction that poeple make efforts to seek gene therapy of lung cancer. The aim of this study is to explore the effects of transfected growth arrest-specific homeobox gene (Gax gene) on the proliferation and expressions of c-fos and c-jun mRNA in A549 cells.</p><p><b>METHODS</b>A549 cells were transfected with Gax gene by adenovirus. Expressions of Gax mRNA and protein were detected by RT-PCR and immunocytochemistry. The expressions of c-fos and c-jun mRNA were evaluated by RT-PCR. The proliferation inhibition effect of Gax transfection on A549 cells was evaluated by MTT assay.</p><p><b>RESULTS</b>Only in the A549 cells transfected with Gax gene the Gax expression was confirmed by RT-PCR and immunocytochemistry. Compared with that in the control group, c-fos and c-jun mRNA level decreased significantly in Gax-transfected A549 cells (t=7.755, P < 0.01; t= 5.938 , P < 0.01). MTT assay showed that the proliferation inhibition rates of A549 cells transfected by Ad-Gax for 24h, 48h and 72h were (47.35±5.36)%, (54.96±1.78)%, and (65.39±5.11)% respectively. And these proliferation inhibition rates were significantly higher than those in the control group (Chi-Square=7.152, 9.431 and 12.847, P < 0.01).</p><p><b>CONCLUSIONS</b>Gax gene can inhibit the proliferation of A549 cells. Its molecular mechanism may be through down-regulating the expressions of c-fos and c-jun.</p>
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<p><b>BACKGROUND</b>In recent years, many progresses have been made in molecular target therapy for lung cancer, in which anti-angiogenic target therapy is a hot spot drawing researchers' attention. The aim of this study is to explore the expression of canstatin gene transfected into human lymphocytes and its inhibitory effect on growth and metastasis of Lewis lung carcinoma.</p><p><b>METHODS</b>The eukaryotic expression vector of pCMV-Script and the recombinant pCMV-Script/Canstatin vector were separately transfected into lymphocytes by electroporation. The expression of canstatin protein in supernatant of lymphocyues was examined by SDS-PAGE assay. Furthermore, Lewis lung carcinoma cells were subcutaneously inoculated to C57BL mice to make animal model of tumor. When the transplanted tumors on the mice developed to 1cm³, the 30 mice were randomized into 3 groups, which were injected with 0.2mL supernatant of lymphocytes transfected with recombinant vector or naked vector, or 0.2mL NS respectively. After the treatment for 14 days, the size and pathological section of subcutaneous tumors were observed, and the number of pulmonary metastatic node was calculated.</p><p><b>RESULTS</b>Canstatin protein was found in supernatant of the lymphocytes in the recombinant vector group by SDS-PAGE assay. After the treatment, the tumor size in the recombinant vector group (1.49cm³±0.18cm³) was significantly smaller than that in the naked vector group (2.44cm³± 0.19cm³) and NS group (2.53cm³±0.18cm³) (P=0.000). The numbers of pulmonary metastatic node were 3.40±1.14, 7.60±2.61 and 7.60±2.41 in the recombinant vector group, naked vector group and NS group respectively (recombinant vector group vs the other two groups, P=0.013).</p><p><b>CONCLUSIONS</b>The pCMV-Script/Canstatin vector can express canstatin protein in human lymphocytes. Canstatin has strongly inhibitory effect on growth and metastasis of mouse Lewis lung carcinoma.</p>
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Canstatin protein, a newly found angiogenesis inhibitor, has powerful anti-angiogenesis effect. Canstatin is the N terminal fragment of collagen IV alpha2 chain NC1 domain. Its distinct anti-cancer effect in mouse model and low toxicity has not only made it a promising new anti-cancer drug candidate, but also drawn much attention of researchers. The detection, denomination, biological characters and mechanism of canstatin protein, and also the prospect of its application were summarized.
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Animals , Humans , Mice , Angiogenesis Inhibitors , Pharmacology , Antineoplastic Agents , Pharmacology , Collagen Type IV , PharmacologyABSTRACT
<p><b>BACKGROUND</b>Angiogenesis is essential for tumor's growth and metastasis. Canstatin, a newly found potent endogenous angiogenesis inhibitor, has drawn researcher's attention to its powerful biological activities on endothelial cells. The aim of this experiment is to explore the expression and effects of canstatin gene in lung cancer A549 cells and HUV-ECC cells.</p><p><b>METHODS</b>Expression vector of pCMV- Script/Canstatin was transfected into A549 and ECC cells by electroporation, and the positive clone was screened by G418. Growth characteristics of the two cell lines were compared before and after transfection. Expression of canstatin protein in supernatant was examined by SDS-PAGE assay, and cell cycles of the two cell lines were analysed by flow cytometry.</p><p><b>RESULTS</b>The expression of canstatin gene was found in supernatant of the transfected A549 cells and ECC cells. The apoptotic rate in the transfected ECC cells (16.04%) was significantly increased compared with that of the naked plasmid control group (0.43%) and parental cell group (2.92%) (P < 0.01). The growth of the transfected ECC cells was significantly inhibited (P < 0.01). The apoptotic rate in the transfected A549 cells (0.19%) showed no marked difference from the naked plasmid control group (0.13%) and parental cell group (0.07%) (P > 0.05). No significant difference in cell growth was found among the transfected A549 cell, naked plasmid control and parental cell groups.</p><p><b>CONCLUSIONS</b>The results indicate that canstatin gene can express in lung cancer A549 cell line and HUV-ECC cell line, and it can specifically inhibit proliferation of endothelial cell and induce its apoptosis.</p>
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BACKGROUND: Chronic obstructive pulmonary disease(COPD) is characterized of chronic inflammation in airway, pulmonary parenchyma and pulmonary vessels. The mechanism of the increment and activity changes of these inflammatory cells is unclear at present.OBJECTIVE: To study the apoptotic character of peripheral blood polymorphonuclear neutrophils(PMNs) and its relationship with COPD to provide a reference for early intervention and function surveillance for COPD patients.DESIGN: An observatory comparative study based on COPD patients and healthy population as controls.SETTING: Department of pulmonary medicine in a military medical university of Chinese PLA affiliated hospital.PARTICIPANTS: Totally 98 COPD patients were admitted by the Department of Pulmonary Medicine, Research Institute of Surgery, Daping Hospital, Third Military Medical University of Chinese PLA between February 2003 and December 2003 due to COPD acute attack. Eighteen patients including 12 males and 6 females aged between 48 and 70 years old [mean of(56 ± 7) years old]were randomly selected into COPD group according to random number table.Totally 14 healthy adults including 10 males and 4 females aged between 50 and 70 years old [mean of (59 ± 8) years old] who were individuals came for physical check up in our hospital were selected in control group.METHODS: PMNs were separated from peripheral blood by density gradient centrifugation. The dynamic changes of PMNs apoptosis in peripheral blood was observed by flow cytometer and TUNEL method.MAIN OUTCOME MEASURES: Comparison of PMNs apoptotic rate in peripheral blood among groupsRESULTS: As indicated by flow cytometric analysis, PMNs apoptotic rate at early apoptotic phase in COPD patients at paracmasis was(8.5 ± 1.3)%,which was significantly lower than(12.5 ± 1.8)% of normal control group( t=6.25, P ＜ 0. 01); PMNs apoptotic rate was(5.1 ±0.6)% at acute aggravation stage, which was significantly lower than that of paracmasis group ( t =5.66, P ＜001). As indicated by TUNEL analysis, PMNs apoptotic rate at paracmasis was(12.42 ±2.7)% , which was significantly lower than (21.5±4.8)% of normal control group(t=5.76, P ＜ 0.01); PMNs apoptotic rate was(4. 9 ±0.4)% at acute aggravation stage, which was significantly lower than that of paracmasis group( t = 6. 12, P ＜ 0. 01 ) . PMNs changes at the late phase of apoptosis/necrosis had a contrary tendency, i. e.,PMNs rate at late apoptotic phase/necrosis was(2. 8 ± 0.5)% in COPD patients at paracmasis, which was significantly higher than(1. 3 ±0.4)% of normal control group ( t= 6. 37, P ＜ 0. 01 ); PMNs rate was (3.7 ± 0. 3) % at acute aggravation stage, which was significantly higher than that of paracmasis group(t=5.81, P ＜0.01).CONCLUSION: PMNs abnormal apoptosis might be an important reason that induces PMNs aggregation in airway and lung tissues in COPD. This process might have an important significance in the generation and development of chronic airway inflammation, which provides an etiologic basis for the primary rehabilitative intervention of COPD.
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Objective To explore the effects of antisense vector of annexinⅡ gene on the growth of SPC A 1, a human lung cancer cell line. Methods The total RNA was isolated from human lung cancer cell line SPC A 1 and the target DNA fragments were amplified by RT PCR. The antisense expression vector was constructed by double restriction endonuclease cleavage directional clone method. Annexin Ⅱ antisense expression vector was introduced into SPC A 1 cells by liposome transfection reagent. The expression of annexin Ⅱ mRNA was analyzed by semi quantitative RT PCR. The effects of antisense vector of annexinⅡ gene on the growth of SPC A 1 were observed. Results The antisense vector of annexinⅡ gene was constructed and introduced into SPC A 1 cells successfully. Semi quantitative RT PCR showed that the annexin Ⅱ mRNA expression reduced by about two thirds in the transfected cells as compared with that in the untransfected cells. Compared with the untransfected cells, transfected cells decreased significantly in cell growth, clone formation efficiency in plating and DNA synthesis. Cell cycle was blocked in G 0 G 1 phase. Conclusion Annexin Ⅱ could promote the growth of lung cancer cells and may be helpful for the development of lung cancer.
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Objective To explore the roles of bacterial infection in the pathogenesis and progression of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Methods The clinical data of 604 patients with ALI or ARDS hospitalized from April 1991 to March 2001 were analyzed. Results (1) The cause of direct lung injury was predominantly ascribed to lung infection, whereas indirect lung injury was due to sepsis. (2) The gram positive cocci (50.76%) and gram negative bacilli (40.15%) in the isolated pathogenic bacteria from patients were approximately similar. Furthermore, Staphylococcus aureus and Pseudomonas aeruginosa were the first and second pathogenic bacteria, respectively. (3) The incidences of ALI and ARDS in infected patients significantly increased with the grade elevation of systemic inflammatory response syndrome (SIRS) ( P
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Objective To investigate the characteristics of the acute lung injury induced by oleic acid (OA) and lipopolysaccharide (LPS) in rats. Methods Wistar rats were injured with OA (0.2 mL/kg) and LPS (2 mg/kg) to establish the acute lung injury (ALI) model. The indexes of respiratory rate, PaO 2, wet weight/dry weight (W/D) of lung lobes, plasma IL 13, and pathological changes were observed. Results Acute respiratory distress syndrome (ARDS) was found in rats treated with OA LPS. The level of PaO 2 was lower than 8 kPa at the early stage. Increased death rate, significantly increased water content in the lungs, more serious pulmonary edema and infiltration of inflammatory cells accompanied by formation of hyaline membrane, and significantly increased plasma IL 13 content were also found. There were significant changes of the above indices, especially in OA LPS/4 h group. Conclusion OA LPS might cause serious ALI/ARDS. Injury due to second time low dose OA LPS after the first time injury may induce ARDS, which may be associated with the abnormally increased level of anti inflammatory cytokines. There is a relative sensitivity between the two injuries.
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Objective To investigate the effects of tumor necrosis factor ? (TNF ?) on ? adrenoceptor (? AR) and ? AR related G protein coupled receptor kinases (GRKs) in rat pulmonary microvascular endothelial cells (PMVECs) as well as the interfering action of anisodamine. Methods Radio ligand binding assay was used to measure the maximal binding capacity (B max ) changes of ? AR in rat PMVECs after treatment with TNF ?. The effects of TNF ? and ? AR related GRKs expression at the protein level were observed by Western blotting. Results B max of ? AR in normal rat PMVECs was (5.58?0.31) fmol/10 5 cells. B max of ? AR in TNF ? group decreased significantly as compared with that in the normal control group, but no significant difference was found between the normal control group and TNF ?+anisodamine group. The expression of GRK2 in rat PMVECs was positive, but expression of GRK3, GRK5, and GRK6 were negative. The expression of GRK2 in TNF ? group and TNF ?+anisodamine group increased significantly as compared with that in the normal control group, but no significant difference was found between the TNF ? group and the TNF ?+anisodamine group. Conclusion GRK2 but not GRK3, GRK5, or GRK6 is expressed in rat PMVECs. The increased expression of GRK2 induced by TNF ? in rat PMVECs might promote the phosphorylation of ? AR, leading to ? AR internalization and decoupling with G protein, which might be the main mechanism of down regulation of ? AR induced by TNF ?. Anisodamine might inhibit the down regulation of ? AR through other mechanism instead of inhibiting the increase of GRK2 expression.
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Objective To explore the effects of polyclonal antibody to lipopolysaccharide binding protein (pLBPab) on IL 10 and IL 18 mRNA expressions of alveolar macrophages in lipopolysaccharide LPS induced acute lung injury in rats. Methods A total of 40 male Wistar rats were randomly divided into 5 groups: normal control (A), LPS treated group (B), group of pLBPab preconditioning at 30 min before injection of LPS (C), group of treatment with LPS and pLBPab (D), and group of pLBPab preconditioning at 30 min after injection of LPS (E). mRNA expressions of IL 10 and IL 18 in the alveolar macrophages in each group were measured by semi quantitative reverse transcription polymerase chain reaction (RT PCR). Results The IL 10 and IL 18 mRNA expressions were highly increased respectively in the alveolar macrophage (AM?) stimulated with single LPS, but they were significantly decreased in the AM? after stimulation with LPS + pLBPab, particularly stimulation with pLBPab 30 min before LPS injection. Conclusion pLBPab can decrease the mRNA expressions such as IL 10 and IL 18 by alveolar macrophages in acute lung injury in rats induced by LPS, and LBP antibody could be used to cure some diseases such as SIRS, acute lung injury, ARDS, and septic syndrome.
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Objective To investigate the changes of plasma interleukin 4 (IL 4) in rats with acute lung injury (ALI) induced by lipopolysaccharide (LPS) and to explore the relationship between IL 4 and ALI. Methods A total of 120 Wistar rats were randomly divided into 2, 4, 6, and 8 mg/kg groups according to different doses of LPS administration at each observing time point. A control group (NS), receiving saline injection, was also employed. The indexes of respiratory rate, PaO 2, wet weight/dry weight (W/D) of lung lobes, and pathological changes were observed at 1, 2, 4, and 6 h after injury. The plasma IL 4 content was detected by enzyme linked immunosorbant assay. Results ① Various degrees of ALI in rats were induced by different doses of LPS. Acute respiratory distress syndrome (ARDS) was induced under the condition of LPS ≥6 mg/kg. ② LPS could induce increased plasma IL 4 in rats. The peak value of plasma IL 4 in rats increased significantly under the condition of LPS ≥6 mg/kg. Conclusion ① ALI model can be duplicated by injection of LPS. ② LPS ≥6 mg/kg is the critical dosage for ARDS in rats. ③ The obvious increase of plasma IL 4 may be associated with the occurrence of ALI/ARDS.
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Objective To study the expression of Gq protein in bronchopulmonary tissues of rats of chronic obstructive pulmonary disease (COPD) model and the roles of inflammation in airway of COPD rats. Methods A total of 44 Wistar rats were divided randomly into 4 groups: nonsmoking control group, 1 month smoking group, 2 month smoking group, and intervention group (dexamethasone + smoking for 2 months). The pathological changes of lung tissues and the total and differential count of white blood cells in bronchoalveolar lavage fluid (BALF) in all groups were observed. The expression of Gq in bronchopulmonary tissues was detected by immunohistochemical method and Western blot analysis. Results More significant increases in total number of leukocytes and neutrophils in BALF were found in the model group than those in the control group. Gq was mainly expressed in airway epithelial cells, inflammatory cells, and pulmonary capillary endothelia. Weak expression of Gq was found in bronchopulmonary tissues in the control group, but overexpression of Gq in the model group. The ratios of Gq positive cells in bronchopulmonary tissues were significantly correlated with the number of white blood cells and neutrophils in BALF. The levels of expression of Gq were significantly higher in the model groups and intervention group than those in the control group. More significant decrease in Gq expression was found in the intervention group as compared with that in 3 month smoking group. Conclusion Gq may be involved in the process of airway inflammation in COPD. Inhibition of the Gq overexpression might be a new approach to the treatment of COPD. Corticosteroid might have some effects on the inhibition of the airway inflammation.
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Objective To establish a small cell lung cancer (SCLC) multidrug resistance (MDR) cell line SH77/CDDP and analyze its biological properties. Methods The SCLC MDR cell line SH77/CDDP was established by increasing gradually the dose of cisplatin, the first line chemotherapeutic drug for lung cancer. The chemosensitivities of SH77/CDDP and its parental cell line to 7 chemotherapeutic drugs were tested. Changes in cellular morphology and ultrastructure were observed. The cell growth curve and cell cycle were also determined. Results SCLC MDR cell line SH77/CDDP having different drug resistance to the 7 chemotherapeutic drugs was established successfully. Compared with that of its parental cell, the size of MDR cell was a bit bigger. The ratio of nucleus to cell plasma decreased and mitochondria, Golgi bodies, rough endoplasmic reticulums and free ribosomes increased. The finger like apophysis was obvious. The rate of cell proliferation of SH77/CDDP was similar to that of SH77, but the number of cells in S phase increased( P