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BACKGROUND: Recombinant human granulocyte-macrophage colony stimulating factor (rhGM-CSF) could stimulate the proliferation of fibroblasts, keratinocyte and skin mucosae cells to different degrees.OBJECTIVE: To observe the effect of rhGM-CSF on the healing of drug exosmose induced skin ulcers.DESIGN: A randomized and controlled animal experiment.SETTING: Department of Respiratory Medicine, Xijing Hospital, Fourth Military Medical University of Chinese PLA.MATERIALS: This experiment was carried out at the Department of Respiratory Medicine, Xijing Hospital, Fourth Military Medical University of Chinese PLA from June to November 2004. Totally 20 male Kunming white mice, with body mass of 18 to 24 g, were chosen.METHODS: Prepared skin ulcers animal models were randomly divided into control group and treated group with 10 white mice in each group.Mice in the control group were given 1mg phentolamine ,20 mg lidocaine and 1mg dexamethasone diluted by normal saline to 0.5 mL ,then sealed up , once a day for 7 days; 25 μg rhGM-CSF was diluted by normal saline to 0.5 mL , then the solution was injected into the periphery of ulcers of mice in treated group , once every other day, for 7 days. Healing time and histological change of skin tissue at ulcer were observed.MAIN OUTCOME MEASURES: To observe the effect of rhGM-CSF on the healing time of drug exosmose induced skin ulcer and anabrosis and histological changeRESULTS: Totally 20 mice entered the stage of result analysis. ①Healing time: the healing time of ulcer and erosion was significantly longer in control group than in treated group [(20-24,8-12)d,t=2.264,P=0.01];②Histological observation: hyperplasia of granulation tissue was not obviously on 7 days after treatment in control group; Hyperplasia of granulation tissue appeared and the newly born blood vessel was abundant on 7 days after treatment in the treated group.CONCLUSION: rhGM-CSF can promote the wound healing of drug induced anabrosis and ulcer.
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Objective To investigate possible intracellular s ignal molecules involved in TGF-?-induced airway smooth muscle cell proli feration in rats. Methods The cultured airway smooth muscle cells were divide d into 3 groups: control group (20 mL?L -1FCS/DMEM), 10 ?g?L -1 TGF-?1 group and 10?g?L -1 TGF-?1 /U-0126 (1 ? mol?L -1) group. The proliferation of ASMCs was detected by MTT. Exp ression of phospho-p42/p44 extracellular signal-regulated kinase (ERKs) with i mmunocytochemistry were examined in different groups. A values were detected by image analysis. Results By MTT, A values of 10?g?L -1 TGF- ?1 group (0.36?0.043) were significantly higher than those of control grou p (0.126?0.052, t=5.44,7.62, P
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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 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 obtain a vaccine with sLAG-3 as immunoadjuvant and investigate its biologic activity in order to establish the safe and effective way for asthma as one of the specific immunotherapy.METHODS: The coding sequence of LAG-3 was amplified by polymerase chain reaction,the expression vector pcDNA-sLAG-3-Ig was constructed by inserting the PCR products of sLAG-3 and Fc sequence of IgG.With electroporation transfection,pcDNA-sLAG-3-Ig was transfected into COS-7 cells and its biologic activity was investigated by Western blotting analysis.RESULTS: By temperature induction,the LAG-3-Ig was highly expressed in E.coli DH5?.LAG-3-Ig fusion protein was observed by SDS-PAGE and Western blotting,the results showed that the LAG-3-Ig protein was an antagonist of the IL-4-induced synthesis of IgE in B cells.CONCLUSION: A new vaccine with sLAG-3 as immunoadjuvant was obtained.It could inhibit synthesis of IgE in B cells.Thus,LAG-3-Ig would be hopeful to establish the safe and effective way for asthma as one of the specific immunotherapy.
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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 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.