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作 者:魏路清[1] 李振华[1] 康健[1] 侯显明[1] 于润江[1]
机构地区:[1]中国医科大学附属第一医院呼吸疾病研究所,沈阳110001
出 处:《中华结核和呼吸杂志》2006年第6期399-402,共4页Chinese Journal of Tuberculosis and Respiratory Diseases
摘 要:目的探讨特发性肺纤维化(IPF)患者支气管肺泡灌洗液(BALF)及血清中基质金属蛋白酶9(MMP9)、基质金属蛋白酶组织抑制剂1(TIMP1)水平的变化。方法2001至2004年用酶联免疫吸附(ELISA)法检测30例IPF患者BALF及血清中MMP9和TIMP1的水平,同时行肺高分辨率CT(HRCT)及肺功能检查。健康非吸烟的自愿献血者30名,为血清对照组。以胸痛为自觉症状在我院自愿进行纤维支气管镜及BALF检查,经体检及X线检查证实为健康者13名,作为BALF对照组。结果IPF患者BALF及血清中MMP9水平为(245±26)和(203±32)ng/L,对照组为(205±22)和(186±16)ng/L,两组相比差异无统计学意义;IPF组BALF及血清中TIMP1水平[(522±81)、(166±29)ng/L]高于对照组[(201±31)、(87±16)ng/L],差异有统计学意义;IPF组BALF及血清中MMP9/TIMP1比值(0.53±0.18,1.5±0.3)低于对照组(1.06±0.38,2.6±0.5)。HRCT、肺功能评分及BALF中上述指标与MMP9无明显相关性,与TIMP1呈正相关,与MMP9/TIMP1比值呈负相关。结论IPF患者肺纤维化的发生与TIMP1水平升高及MMP9/TIMP1比值降低对细胞外基质降解的抑制有关,后者可能意义更大;患者肺影像学及肺功能变化可能也与此有关。Objective To detect the levels of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metaUoproteinase-1 ( TIMP-1 ) in the bronchoalveolar lavage fluid (BALF) and the serum of patients with idiopathic pulmonary fibrosis (IPF), and to evaluate the significance of the changes in the pathogenesis of IPF. Methods Enzyme-linked immunoadsordent assay (ELISA) was used to detect MMP-9 and TIMP-1 in the BALF and serum of 30 patients with IPF. Results The levels of MMP-9 in the BALF and serum of the patients showed no significant difference as compared with those of the control group . The levels of TIMP-1 in the BALF [(522±81) ng/L] and serum [(166±29) ng/L] of the patients were higher than those [ (201±31), (87±16) ng/L]of the control group (P 〈0. 01). The ratios of MMP-9/ TIMP-1 in the BALF(0. 53± 0. 18 ) and serum (1.5 ± 0. 3 ) of patients with IPF were lower than those (1.06±0.38, 2.6±0.5) of the control group(P〈0.01, 〈0.05). TIMP-1 in the BALF of the patients showed a strong positive correlation with chest CT fibrosis and pulmonary function test scores ( P 〈 0. 01 ), while MMP-9/TIMP-1 in the BALF had negative correlation with them (P 〈 0. 01 ). Conclusion Pulmonary fibrosis may be associated with increased TIMP-1 and decreased MMP-9/TIMP-1, which is able to inhibit the degradation of extracellular matrix.
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