Respiratory medicine · 2010
Advanced glycation end products and its receptor (RAGE) are increased in patients with COPD.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Wu Lian, Ma Li, Nicholson Louise F B, Black Peter N
Аннотация
UNLABELLED: Advanced Glycation End products (AGEs) are the products of nonenzymatic glycation and oxidation of proteins and lipids. Formation of AGEs is increased in response to hyperglycaemia, reactive oxygen species and ageing. AGEs are proinflammatory and can modify the extracellular matrix. RAGE (Receptor for Advanced Glycation End Products) mediates some of the effects of AGEs.
METHODS: Formalin-fixed lung tissue from patients who had lobectomy for bronchial carcinoma was used to investigate the presence of AGEs and RAGE. Subjects were divided into those with COPD and controls. Immunostaining for AGEs and RAGE was performed and the intensity of staining measured.
RESULTS: Subjects with COPD and controls were similar in age and smoking history but FEV(1)% predicted was lower for COPD than controls. Intensity of staining for AGEs was greater in the airways (p = 0.025) and alveolar walls (p = 0.004) in COPD. Intensity of staining for RAGE was also significantly increased in alveolar walls (p = 0.03) but not the airways. FEV(1)% predicted was correlated with the intensity of staining for AGEs in the airways and alveoli.
CONCLUSIONS: The increased staining for both AGEs and RAGE in COPD lung raises the possibility that the RAGE-AGEs interaction may have a role in the pathogenesis of COPD.
METHODS: Formalin-fixed lung tissue from patients who had lobectomy for bronchial carcinoma was used to investigate the presence of AGEs and RAGE. Subjects were divided into those with COPD and controls. Immunostaining for AGEs and RAGE was performed and the intensity of staining measured.
RESULTS: Subjects with COPD and controls were similar in age and smoking history but FEV(1)% predicted was lower for COPD than controls. Intensity of staining for AGEs was greater in the airways (p = 0.025) and alveolar walls (p = 0.004) in COPD. Intensity of staining for RAGE was also significantly increased in alveolar walls (p = 0.03) but not the airways. FEV(1)% predicted was correlated with the intensity of staining for AGEs in the airways and alveoli.
CONCLUSIONS: The increased staining for both AGEs and RAGE in COPD lung raises the possibility that the RAGE-AGEs interaction may have a role in the pathogenesis of COPD.