Objective To summarize the research progress in antitumor mechanism of non-steroidal anti-inflam-matory drugs. Methods The domestic and international published literatures about antitumor mechanism of non-steroidal anti-inflammatory drugs in recent years were reviewed. Results The antitumor mechanism of non-steroidal anti-inflam-matory drugs was multistrata and multidigit. Conclusion Non-steroidal anti-inflammatory drugs can be used to prevent the development of colorectal cancer and also be a adjuvant therapy after radical operation for colorectal cancer.
ObjectiveTo investigate the changes of diamine oxidase(DAO) and endotoxin(ET) during the treatment of systemic inflammatory response syndrome with human growth hormone and the relationship between human growth hormone and intestinal mucosal barrier injury. MethodsOne hundred and fortysix patients with systemic inflammatory response syndrome were randomly divided into operative group and nonoperative group, which were again randomly divided into the study group and control group.Plasma concentration of DAO and ET were determined before the treatment and 1 week after the treatment.ResultsPlasma concentration of DAO and ET in study group decreased after treatment with significant difference (P＜0.05，P＜0.01).ConclusionHuman growth hormone can protect intestinal mucosa barrier.
To evaluate the process from systemic inflammatory response syndrome (SIRS) to multiple organ dysfunction syndrome (MODS) and probe the therapeutic strategies for elderly patients, we retrospectively studied the clinical data of SIRS and MODS in 292 elderly patients with surgical abdominal emergency. Results: On admission, the morbidity rate of SIRS was 41.1%. Afterwards the morbidity rate of MODS was 14.2%, and the mortality rate of the elderly patients with SIRS was 11.7%. After 48 hours of therapy, MODS was developed in 40.5% of the cases also with SIRS. Of all the 292 elderly patients, 19 cases (6.5%) developed MODS and 16 patients (84.2%) died. Conclusion: The outcome of the patients with surgical abdominal emergency may be improved if SIRS is early diagnosed, the cause of SIRS after 48 hours therapy is well defined and the body inflammatory response is properly regulated.
The synthesis and secretion of inflammatory cytokines in the monocytes of 68 cases of multiple system organ failure (MSOF) patients was investigated by the method of MTT stained in cytokines dependent defferential cell strain. The data showed that the serum levels of tumor necrosis factor, interleukine 1 and interleukine 6 were increased (Ｐ＜0.01) in the monocytes of MSOF patients. The synthesis and secretion of these inflammatory cytokines gradually increased in the monocytes after onset of MSOF. After 5 days of treatment with antibiotics and electrolytes intravenous infusion, the secretion of TNF, IL-1 and IL-6 were decreased respectively. These results suggested that the TNF, IL-1 and IL-6 are integrated into system inflammatory responese and caused the injury to the tissues and organs. The production levels of these cytokines can be regarded as the index of MSOF and its severity.
Objectives To explore the expression of macrophage inflammatory protein-1beta (MIP-1β) in patients with none-small cell lung cancer (NSCLC) of different pathological types and its association with cancer clinical stages and metastasis of lymph nodes.Methods MIP-1β mRNA from fresh lung tissue of 38 NSCLC patients was amplified by RT-PCR and half-quantified.Immunohistochemical technique was performed to find out the expression of MIP-1β in paraffin-embedded lung tissue from 66 patients with NSCLC.The area and degree of stain were evaluated to determine the positive rate，which was compared between with or without metastasis of lymph nodes，different pathological types and TNM clinical stages.Results MIP-1β protein was found in cytoplasm of malignant cells of squama cell cancer and adenocarcinoma without significant difference between them，while not found in bronchus-alveolus cell cancer.The MIP-1β mRNA expression in squama cell cancer and adenocarcinoma were significant higher than which in bronchus-alveolus cell cancer without significant difference between each other.The positive rates of MIP-1β in lung cancer of Ⅰ，Ⅱ and Ⅲ stages were 74.2%，29.4% and 85.7% respectively，which of Ⅰ and Ⅲ stages cancer were significant higher than Ⅱ stage without significant difference between each other.The positive rates of MIP-1β in lung cancer with or without metastasis of lymph nodes were 45.8% and 76.3% respectively with significant difference between them.Conclusion MIP-1β is expressed in lung cancer cells and relates to the pathological type，TNM stage and the metastasis of lymph nodes.
Objective To investigate the mRNA and protein expression of human β-defensin-2 (hBD-2) induced by lipopolysaccharide (LPS)，IL-1β and TNF-α in human airway primary epitheliums.Methods The bronchial primary epitheliums from human were stimulated with LPS，IL-1β and TNF-α respectively and then were harvested for hBD-2 expression detection.The mRNA expression of hBD-2 was detected by RT-PCR，and the protein expression by immunocytochemistry and western blot.Results There was a small expression of hBD-2 mRNA in human airway primary epitheliums before stimulation.The hBD-2 mRNA expression was significantly increased after 3 hours of LPS，IL-1β and TNF-α stimulation respectively and the expression increasement was in a dose dependent manner.The hBD-2 protein could be detected in cytoplasm after 4 hours of LPS (0.1 μg/mL)，IL-1β (1 ng/mL) and TNF-α (10 ng/mL) stimulation.Conclusions LPS and proinflammatory cytokines can induce the mRNA and protein expression of hBD-2 in a short time.The expression of hBD-2 may play an initial defense role against bacterial invasion.
Objective To investigate the effects of mechanical ventilation on lung pathology and concentration of proinflammatory cytokines in rats.Methods Forty-five healthy Sprague-Dawley rats were randomly divided into three groups with 15 rats each group，ie.a control group(No mechanical ventilation)，a high tidal volume group(VT 34 mL/kg，RR 30 bpm) and low tidal volume group(VT 8 mL/kg，RR 60 bpm).Results There were enlarged alveolar spaces，interalveolar septum collapse，swollen and spotty hemorrhages，inflammatory cell infiltration in the ventilation groups，which was more serious in the high tidal volume group.Lung wet-to-dry weight ratio of high tidal volume group was significantly higher than that of other groups（both Plt;0.05）.The concentrations in both macrophage-inflammatory protein-2（MIP-2）and tumor necrosis factor-α(TNF-α) of bronchoalveolar lavage fluid(BALF) and blood samples was significantly higher in two ventilation groups than the control group（Plt;0.05），which were higer in the high tidal volume group than in the low tidal volume group（Plt;0.05）.Conclusions These results indicate that mechanical ventilation can cause lung injury，which is more serious in high tidal volume ventilation.And mechanical ventilation-induced lung injury can cause proinflammatory cytokines release，with different levels in bronchoalveolar lavage fluid and blood samples.
Objective To study the role of E-selection and macrophage inflammatory protein-2（MIP-2） in the airway inflammation in a rat model of chronic obstructive pulmonary disease（COPD）.Methods Twenty-four male SD rats were randomly divided into a normal control group and a COPD group.The rat model of COPD was established by exposure to cigarette smoking.Lung function，pathologic features of lung tissues and inflammatory cell differentials in bronchoalveolar lavage fluid（BALF） were investigated.Immunohistochemistry was employed to examine the expression of E-selection in lung tissue.The levels of MIP-2 in BALF，serum and lung tissues were measured with ELISA.Results The changes in histopathology and pathophysiology in the rat COPD model were similar to those in COPD patients.The expression of E-selection on bronchopulmonary vein endothelial cells of the COPD group significantly increased as compared with the normal control group（Plt;0.05） and was positively correlated with the neutrophil counts in BALF in the COPD group（ｒ=0.809，Plt;0.01）.The levels of MIP-2 in BALF and lung tissues in the rats with COPD were signicantly higher than those in normal rats，both of which were positively correlated with the neutrophil counts in BALF in the COPD group（r=0.893，Plt;0.01；r=0.716，Plt;0.05）.Conclusion Both E-selection and MIP-2 may be involved in the process of airway inflammation in COPD.
Objective To investigate the percentage of CD4+CD25+ Treg in peripheral blood of patients with severe multiple trauma and systemic inflammatory response syndrome（SIRS） and its effects on cellular immunity and secondary infection.Metheds Peripheral blood of 23 patients with severe multiple trauma was collected in 24 h after SIRS was diagnosed，and flow cytometry was used to determine the percentage of CD4+CD25+ Treg and CD4/CD8 ratio.Simultaneously，in order to explore the cell proliferation，silver staining was used to determine Ag-NORs of leukomonocyte in peripheral blood represented by IS%.In order to investigate the infection in patients，sputum and secretion sample were collected for bacteriological examination on 1 and 5 day after SIRS was established.Forty healthy volunteers were enrolled as control.Results Compared with the control，the percentage of CD4+CD25+ Treg was significant higher[（14.21±3.43）% vs（9.53±3.22），Plt;0.01] and the ratio of CD4/CD8 and IS% were significant lower in patients with severe multiple trauma[（5.94±0.66）% vs（6.74±0.95）%，（1.22±0.25）% vs（1.72±0.36）%，respectively，both Plt;0.01].In those patients（n=14） who developed secondary infection，Treg% was significant higher [（18.69±4.21）% vs（12.58±2.49）%，Plt;0.01]，while IS% and CD4/CD8 were significant lower [（5.79±0.68）% vs（6.15±0.57）%，（1.15±0.25）% vs（1.39±0.25）%，both Plt;0.01].compared to the patients without secondary infection Conlusion CD4+CD25+ Treg is valuable to estimate the cellular immunity and predict secondary infection in patients with severe multiple trauma.
Objective To observe the effects of mechanical stretch on cytokines release from alveolar macrophages( AMs) and the expression of macrophage inflammatory protein-2( MIP-2) induced by lipopolysaccharide( LPS) . Methods AMs were divided into the following groups: ①AMs were subjected to 20% elongation by Flexercell 4000T cell stress system for 24 hours and the supernatant was collected to detect the levels of TNF-α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12, IFN-γ, macrophage inflammatory protein-1α( MIP-1α) , MIP-2, monocyte chemoattractant protein-1( MCP-1) , granulocyte /macrophage colony stimulating factors( GM-CSF) , interferon inducible protein-10( IP-10) , regulated on activation in normal T-cell expressed and secreted( Rantes) and keratinocyte chemoattractant( KC) , by using LiquiChip system. ② AMs were subjected to 5% , 10% , 15% and 20% elongation for 24 hours and the supernatant was collected to detect the levels of MIP-2. ③AMs were subjected to 20% elongation and MIP-2 in supernatant was detected 1, 3,6, 12, and 24 hours later. ④ AMs were subjected to 20% elongation and/ or LPS at a concentration of 10 ng/mL, and MIP-2 in supernatant was detected 24 hours later. Unstretched AMs were used as control in all kind of test. Results ①The levels of IL-1β, IL-6,MIP-2, MCP-1, IFN-γand IP-10 secreted by stretched AMs were 8. 7, 4. 3, 38. 6, 4. 8, 14. 2 and 5. 0 times those of the control group( all P lt; 0. 001) . ② The levels of MIP-2 secreted by AMs subjected to 10% , 15% and 20% elongation were ( 480. 5 ±93. 1) pg /mL,( 806. 3 ±225. 9) pg/mL and ( 1335. 7 ±18. 5) pg/mL respectively, all significantly higher than those oft he control group [ ( 34. 6 ±11. 4) pg/mL, all P lt;0. 001] . ③ Three hours after the stimulation of stretch the level of MIP-2 began to increase gradually. And 6, 12, and 24 hours after the stimulation the levels of MIP-2 secreted by the AMs were ( 819. 4 ±147. 5) pg/mL, ( 1287. 6 ±380 ±3 ) pg/mL and ( 1455. 9 ±436. 7) pg/mLrespectively, all significantly higher than those of the control group[ ( 33. 4 ±10. 2) pg/mL, all P lt; 0. 001] . ④When the AMs were stimulated individually by LPS( 10 ng /mL) or mechanical stretch ( 20% ) , the levels of MIP-2 increased to ( 1026. 3 ±339. 5 ) pg/mL and ( 1335. 7 ±318. 5 ) pg/mL respectively( both P lt; 0. 001) . When the AMs were costimulated by LPS and mechanical stretch, the level of MIP-2 increased to ( 2275. 3 ±492. 1) pg/mL, implicating a synergistic effect between mechanical stretch and LPS ( F = 121. 983, P lt; 0. 001) . Conclusions Mechanical stretch activates AMs to produce multiple inflammatory cytokines and induce AMs to secret MIP-2 in a strength- and time-dependent manner.Mechanical stretch also has synergistic effect with LPS in inducing MIP-2 release, which might play an important role in the development of ventilator-induced lung injury.