共查询到20条相似文献,搜索用时 15 毫秒
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Corticosteroid effects on cell signalling. 总被引:5,自引:0,他引:5
P J Barnes 《The European respiratory journal》2006,27(2):413-426
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Adcock IM Caramori G Barnes PJ 《Respiration; international review of thoracic diseases》2011,81(4):265-284
Both chronic obstructive pulmonary disease (COPD) and lung cancer are major causes of death worldwide. In most cases this reflects cigarette smoke exposure which is able to induce an inflammatory response in the airways of smokers. Indeed, COPD is characterized by lower airway inflammation, and importantly, the presence of COPD is by far the greatest risk factor for lung cancer amongst smokers. Cigarette smoke induces the release of many inflammatory mediators and growth factors including TGF-β, EGFR, IL-1, IL-8 and G-CSF through oxidative stress pathways and this inflammation may persist for decades after smoking cessation. Mucus production is also increased by these inflammatory mediators, further linking airway inflammation to an important mechanism of lung cancer. A greater understanding of the molecular and cellular pathobiology that distinguishes smokers with lung cancer from smokers with and without COPD is needed to unravel the complex molecular interactions between COPD and lung cancer. By understanding the common signalling pathways involved in COPD and lung cancer the hope is that treatments will be developed that not only treat the underlying disease process in COPD, but also reduce the currently high risk of developing lung cancer in these patients. 相似文献
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慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)反应不仅表现为肺部炎症,而且伴随全身性炎症反应.COPD导致的全身不良效应与全身炎症反应密切相关.COPD患者全身炎症程度以一些炎症介质和(或)标志物(如C-反应蛋白,纤维蛋白原,不同的细胞因子,瘦素)的血浆水平升高... 相似文献
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Lakhdar R Denden S Kassab A Leban N Knani J Lefranc G Miled A Chibani JB Khelil AH 《Experimental lung research》2011,37(6):364-375
Chronic obstructive pulmonary disease (COPD) is characterized by systemic and local chronic inflammation and oxidative stress. The sources of the increased oxidative stress in COPD patients derive from the increased burden of inhaled oxidants such as cigarette smoke and other forms of particulate or gaseous air pollution and from the increase in reactive oxygen species (ROS) generated by several inflammatory, immune, and structural airways cells. There is increasing evidence that genetic factors may also contribute to the pathogenesis if COPD, particularly antioxidant genes, which may confer a susceptibility to environmental insults such as cigarette smoke and thereafter development of COPD. Consequently, heme oxygenase-1 (HO-1), superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), microsomal epoxide hydrolase (EPHX1), and cytochrome P450 (CYP) genetic polymorphisms may have an important role in COPD pathogenesis. In this review the authors summarized the most recent findings dealing with these antioxidant genes contributing to the free radical neutralization and xenobiotic enzymes playing a role in different phases of cell detoxification reactions related to the redox status imbalance in COPD, with an emphasis on their possible roles in disease progression. 相似文献
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Houben JM Mercken EM Ketelslegers HB Bast A Wouters EF Hageman GJ Schols AM 《Respiratory medicine》2009,103(2):230-236
Chronic oxidative stress and systemic inflammation contribute to the pathology of several chronic diseases, one among which is chronic obstructive pulmonary disease (COPD). In addition, increased oxidative stress and inflammation have been observed to be negatively associated with telomere length (TL). Our aim was to investigate the TL in COPD patients in relation to pulmonary and extrapulmonary disease severity. Furthermore, based on experimental evidence suggesting the effects of oxidative stress on telomere shortening, we studied the association of TL with the antioxidant enzyme superoxide dismutase (SOD). One hundred and two COPD patients with moderate to severe COPD were studied and compared with 19 healthy age-matched controls. Patients were characterized by elevated levels of inflammatory markers (CRP, sTNF-receptors) and lower SOD-activity than the controls (p<0.001), irrespective of the SOD genotype. TL was negatively associated with age (p<0.01) and was significantly shorter in COPD patients than controls (p<0.05). Within the patient group age-adjusted TL variability could not be explained by lung function and smoking history but a modest association was found with the percentage of fat mass (p<0.05). These data provide evidence for a relationship between a disturbed oxidant/antioxidant balance and telomere shortening and indicate that preservation of fat mass may be protective in delaying telomere shortening in COPD patients. 相似文献
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OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is a slowly progressive condition characterised by poorly reversible airflow limitation associated with an abnormal inflammatory response of the lung. The main causal factors of COPD are chronic oxidative stress as a result of long-term smoking, use of biomass fuels, and air pollution. In this study, basal levels of DNA strand breaks were investigated together with some additional oxidative markers implicating oxidative damage on the other biomolecules such as proteins and lipids in patients with COPD who were exposed to smoking and biomass. MATERIAL AND METHODS: We detected DNA strand breaks in peripheral blood mononuclear leukocytes by using a Single Cell Gel Electrophoresis (also called Comet Assay), plasma protein carbonyl (PC) content by using Reznick and Parker's spectrophotometric method, and lipid peroxidation by measurement of malondialdehyde (MDA) as indexes of oxidative stress in 47 patients with smoking-related COPD and 25 patients with biomass-related COPD and 36 age-and-sex matched control participants. RESULTS: The mean values of DNA strand breaks, MDA and protein carbonyl levels were significantly higher in smoking- and biomass-related COPD groups than in the control group (ANOVA P<0.001, <0.05 and <0.05, respectively). DNA damage levels were also higher in smoking-related COPD group than in biomass-related COPD group (P<0.05). There was a positive relationship between DNA damage and MDA levels in smoking-related COPD group (P<0.05). CONCLUSION: Oxidative stress markers and DNA damage were strongly increased in both patient groups with smoking- and biomass-related COPD. However, DNA is more affected in smoking-related COPD patients than in biomass-related COPD. These data indicate that cigarette smoking is a more significant DNA damaging risk factor than biomass smoke. 相似文献
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van Helvoort HA Heijdra YF Dekhuijzen PN 《Respiration; international review of thoracic diseases》2006,73(2):255-264
Chronic obstructive pulmonary disease (COPD) is no longer seen as a pulmonary disease, but is increasingly associated with systemic effects with important clinical relevance. Systemic immunological changes in COPD patients are characterized by an increased number of circulating inflammatory cells, functional changes of the inflammatory cells, elevated plasma levels of cytokines, and oxidative stress. Physical exercise induces an abnormal systemic inflammatory and oxidative response in COPD patients, which is seen in both the circulation and the peripheral muscles. Although mechanisms and consequences of these effects are not yet fully understood, they could be harmful in COPD patients by inducing damage or functional changes in, for example, skeletal muscles. Whether these changes of the immune system can also affect the susceptibility to infections in these patients is unknown. The concept of COPD as a systemic rather than only a pulmonary disease also opens new perspectives on the development for new therapeutic interventions. The effects of new antioxidative and anti-inflammatory agents are investigated. A better understanding of the complexity of the systemic effects will aid the development of new therapies and management strategies for patients with COPD. 相似文献
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Irfan Rahman 《INT J CHRONIC OBSTR》2006,1(1):15-29
Oxidative stress is an important feature in the pathogenesis of COPD. Targeting oxidative stress with antioxidants or boosting the endogenous levels of antioxidants is likely to be beneficial in the treatment of COPD. Antioxidant agents such as thiol molecules (glutathione and mucolytic drugs, such as N-acetyl-L-cysteine and N-acystelyn), dietary polyphenols (curcumin, resveratrol, green tea, catechins/quercetin), erdosteine, and carbocysteine lysine salt, all have been reported to control nuclear factor-kappaB (NF-κ B) activation, regulation of glutathione biosynthesis genes, chromatin remodeling, and hence inflammatory gene expression. Specific spin traps such as α-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (ECSOD mimetic), porphyrins (AEOL 10150 and AEOL 10113), and a superoxide dismutase mimetic M40419 have also been reported to inhibit cigarette smoke-induced inflammatory responses in vivo. Since a variety of oxidants, free radicals, and aldehydes are implicated in the pathogenesis of COPD, it is possible that therapeutic administration of multiple antioxidants will be effective in the treatment of COPD. Various approaches to enhance lung antioxidant capacity and clinical trials of antioxidant compounds in COPD are discussed. 相似文献
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慢性阻塞性肺疾病(COPD)的发病涉及到多种炎症基因在肺内的表达,组蛋白去乙酰化酶(HDAC)在调控炎症基因的表达中起至关重要的作用。HDAC2的表达和活性在COPD患者肺组织匀浆及肺泡巨噬细胞中明显减少,与肺功能下降程度和气道炎症强度相关;HDAC表达和活性减低部分参与了COPD患者糖皮质激素抵抗的发生;低浓度茶碱可以恢复HDAC的活性,从而增加对糖皮质激素的敏感性。 相似文献