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AIM: To observe the effect of aminoguanidine (AG) on hemodynamics and lung capillary permeability in acute lung injury (ALI) in rabbits. METHODS: 24 rabbits were equally divided into four groups: saline group, endotoxin group, AG group and AG plus endotoxin group. In AG plus endotoxin group, endotoxin was injected to animals to make an ALI model, 25mg/kg AG was injected following that and let this sustain 3 hours. Meanwhile, mean arterial pressure (MAP), mean pulmonary arterial pressures (MPAP) and blood gas analyses were observed during this period. At the end of the experiment, broncho-alveolus lavage was performed, pathologic samples were treated routinely and lung wet weight/dry weight ratio was calculated. RESULTS: After endotoxin injection, MAP and arterial oxygen pressure (PaO 2) decreased, and MPAP increased significantly. The injection of AG had little effect on MAP, but AG could markedly decrease MPAP and increase PaO 2. Cell count in broncho-alveolus lavage fluid (BALF) was less in AG plus endotoxin group than in endotoxin group. Although AG did not affect total protein in BALF, low molecular weight proteins decreased in AG plus endotoxin group by the assay of electrophoresis. Tissue wet weight/dry weight ratio also decreased in this group. Pathologic study showed that there were fewer inflammatory cells and less lung edema in AG plus endotoxin group. CONCLUSION: AG could improve hemodynamics status and attenuate acute lung injury induced by endotoxin in rabbits. [
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AIM: To study the effect of platelet-activating factor(PAF) on proliferation of cultured rat airway smooth muscle cells(ASMCs).METHODS: The cells were divided into control group and PAF group. The cells in PAF group were subdivided into four small groups by concentrations of PAF 10 -6 , 10 -7 , 10 -8 , 10 -9 mol?L -1 , MTT assay was used not only to investigate the effects of PAF on proliferation of ASMC but also to confirm the optimal concentration. Flow cytometry and immuneohistochemistry for proliferating cell nuclear antigen (PCNA) were also used to analyse its function on proliferation of ASMC.RESULTS: PAF (10 -6 -10 -9 mol?L -1 ) stimulated the cell proliferation and 10 -7 mol?L -1 PAF reached the maximal effect. The cell percentage of the ASMCs of 107 mol?L -1 PAF subgroup at G_ 0/1 phase (68.67%) was much lower than that of control group (85.57%, P
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AIM: To observe the inhibitory effect of antisense eukaryotic expression vectors for c-myc on rat airway smooth muscle cells. METHODS: Antisense and sense eukaryotic expression vectors for c-myc pcDNA3-myc-antisense and pcDNA3-myc-sense were constructed. Lipofectin was used to introduce antisense and sense eukaryotic expression vectors for c-myc into rat. The inhibitory effect was assayed by MTT cell proliferation assay. Cell cycles were detected by flow cytometry technology. The expression of c-Myc was detected by immunohistochemistry. RESULTS: The results showed that antisense eukaryotic expression vector for c-myc inhibited rat airway smooth muscle cells proliferation. Rat airway smooth muscle cells were prohibited in S phase and the expression of c-Myc was decreased after antisense eukaryotic expression vectors for c-myc were transfected into cells. CONCLUSION: Antisense eukaryotic expression vectors for c-myc inhibit rat airway smooth muscle cell proliferation. [
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AIM: To observe the antiproliferative effect of c-myc antisense oligonucleotide in rat thymus lymphocytes. METHODS: Rat thymus lymphocytes were separated by Ficoll-Urografin density gradient centrifugation. Lipofectin was used to introduce antisense, sense and mismatched oligonucleotides for c-myc to rat thymus lymphocytes. The antiproliferative effect was assayed by incorporation of -TdR and MTS cell proliferation assay. TR-PCR was used to detect the expression of c-myc mRNA. RESULTS: c-myc antisense oligonucleotide inhibited rat thymus lymphocytes proliferation [(0.14?0.03)A vs (0.32?0.16)A, P
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AIM: To examine whether calcitonin gene-related peptide (CGRP) enhances nitric oxide (NO) level in pulmonary circulation blood and observe the influence of CGRP on mean pulmonary artery pressure (mPAP) in rabbits with acute lung injury (ALI) caused by oleic acid. METHODS: The level of NO was assessed by measuring the presence of nitrite in cervical artery blood by the Griess reaction, mPAP was measured with right ventricular catheter. RESULTS: The level of nitrite in cervical artery blood was significantly increased and the mPAP was markedly reduced after administration of CGRP intravenousely.CONCLUSION: CGRP enhanced the NO level of pulmonary circulation blood and reduces the mPAP significantly in rabbits with ALI.
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AIM: To investigate the relationship between inflammatory cell infiltration and proto-oncogenes expression in asthma. METHODS: Guinea pigs were used as asthma models challenged by ovoglobulin. Dot-blot, Northern-blot and immunochemical techniques were used to detect the expression of c-fos, c-myc, c-jun and c-sis. Inflammatory cell infiltration was showed by pathologic study.RESULTS: c-fos and c-myc mRNA could not be detected or expressed at very low level in control group. Those were greatly increased after the animals are challenged by ovoglobulin. Immunochemical study showed that Fos, Myc, Jun and Sis expressed at low level in control group, and those were increased after the challenge. There was little inflammatory cell infiltration in control group. Lymphocyte, neutrophil and eosinophil were detected immediately after the challenge, a great number of inflammation cells could be seen after 12-24 h of the challenge. Majority of neutrophil and eosinophil were under mucosa or in epithelium in airway. CONCLUSION: Oncogenes expression had strong relationship with airway inflammation.