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作 者:马小兵[1] 李秀玲[2] 孙树勋[3] 杨方[1]
机构地区:[1]华北煤炭医学院病理教研室 [2]开滦医疗集团林西医院 [3]华北煤炭医学院基础医学部,唐山063000
出 处:《中华劳动卫生职业病杂志》2005年第3期203-205,共3页Chinese Journal of Industrial Hygiene and Occupational Diseases
摘 要:目的探讨SiO2是否通过影响矽肺患者肺泡巨噬细胞(AM)基质金属蛋白酶(MMPs)金属蛋白酶组织抑制因子(TIMPs)系统参与矽肺纤维化的发生发展。方法收集矽肺患者的AM,在体外以SiO2(50μgml)和不加血清的DMEM培养基培养2、6、12、18、24、36h,用免疫细胞化学的方法检测AM中MMP9和TIMP1的表达。结果经SiO2刺激的AMMMP9表达明显上调,且随刺激时间不同表达量也不同,于18h达高峰(平均光密度值为0.440±0.021),与同期对照组AM(0.390±0.011)相比,差异有统计学意义(P<0.05);而TIMP1的表达与对照组(平均光密度值分别为0.175±0.019、0.162±0.044)的差异无统计学意义(P>0.05)。结论SiO2可诱导AM高表达MMP9。AM在损伤早期通过产生MMP9而降解基底膜,可能与包括成纤维细胞在内的各种细胞的迁移有关。Objective To study the effect of SiO_2 on the expression of matrix metalloproteinase(MMP) and tissueinhibitor of metalloproteinase(TIMP) in human alveolar macrophages(AMs) associated with the pathogenesis of silicotic fibrosis. Methods AMs were collected from a silicotic patient by brochoalveolar lavage,and exposed to SiO_2 (50 μg/ml),and cultured in DMEM without serum for different time(2,6,12,18,24,36 h).Immunocytochemical method was used to detect the level of expression of MMP-9 and TIMP-1 in AMs. Results The expression of MMP-9 in AMs exposed to silica was up-regulated,and reached the peak at 18 h[average optical density:(0.440±0.021) vs (0.390±0.011),P<0.05].After that,the expression reduced markedly.However,the expression of TIMP-1 of AMs were not significantly different from the control group[average optical density:(0.175±0.019) vs (0.162±0.044),P>0.05]. Conclusion SiO_2 could induce up-expression of MMP-9 in AMs.Degradation of basement membrane by MMP-9 produced by AMs at early stage of lung injury may associate with the immigration of various cells including lung fibroblasts into the injured region.
关 键 词:金属蛋白酶组织抑制因子-1 肺泡巨噬细胞 基质金属蛋白酶-9 二氧化硅 TIMP-1 MMP-9 DMEM培养基 SiO2 免疫细胞化学 矽肺患者 光密度值 矽肺纤维化 成纤维细胞 发生发展 刺激时间 损伤早期 对照组 统计学 AM 表达量 18h
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