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矿物粉尘诱导的肺泡巨噬细胞因子对肺成纤维细胞作用的研究 |
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of 100 μg 3H-TdR and 14C-Pro incorporated 27 952, 13 416 and 18 538 in the group of 200 μg respectively, which were significantly higher than those in the control group. Total HOP levels in the culture media for lung fibroblast enhanced by AM supernatant were 22.41, 24.00 and 21.39 μg/ml, respectively, and was significantly higher than that in the control group (12.91 μg/ml). Release of TNF and IL-6 could be stimulated by mineral dust, such as quartz, asbestos and uranium mineral dust, and their activities were significantly higher than those in the control group, with those of 1 396, 1 198 and 852 U/ml in TNF group and 1 336, 1511 and 1 335 U/ml in IL-6 group, respectively. Proliferation of lung fibroblast and synthesis of collagen could be inhibited by antibody against TNF and interferon-r (gamma), and the effect of the latter was weaker than that of the former on inhibition of fibroblast proliferation and the effect on collagen synthesis was just in the opposite direction. Conclusion Lung fibrosis caused by mineral dust correlated with abnormal expression of TNF and IL-6. Antibody against TNF and gamma interferon could antagonize the effect of NTF and IL-6.
【Key words】 Minerals Dust Macrophages, alveolar
关于石英、石棉和铀矿尘引起肺纤维化的机理至今尚未完全清楚。近年来研究认为,肺泡巨噬细胞(alveolar macrophage，AM)释放的细胞因子,如肿瘤坏死因子(tumor neceosis factor,TNF)、血小板生长因子(platelte derived growth factor,PDGF)、白细胞介素等在尘肺纤维化中起着十分重要作用［1，2］。我们研究了石英、石棉和铀矿粉尘诱导的AM上清液中细胞因子TNF和白细胞介素-6(interleukin-6，IL-6)对肺成纤维细胞的作用以及抗TNF抗体和γ干扰素(interferen-gamma,IFNγ)对活化的肺成纤维细胞的抑制作用，旨在探索AM因子在肺纤维化中的作用，藉以加深了解肺纤维化的发病机理，并为尘肺病的防治提供实验依据。
材料与方法
一、材料
1.粉尘悬液:国际标准石英粉(DQ12)和国际标准温石棉(UICC)由美国NIOSH提供; 铀矿粉尘由中国核工业总公司711矿提供, 含游离SiO2 34 %、U3O8 1%,粒径<5 μm的占91%;二氧化钛(TiO2)由中国预防医学科学院提供, 纯度99%, 粒径<5 μm。称取上述粉尘，用Hank(无Ca2+、Mg2+离子)配成2 mg/ml混悬液，高压灭菌备用，使用前充分混匀。
2.主要试剂:RPMI 1640培养基为美国GIBCO产品,氚-胸腺嘧啶(3H-TdR)由上海原子能研究所提供,14碳-脯氨酸(14C-Pro)由北京原子能研究所提供,四甲基偶氮唑盐(MTT)为Fluca公司产品,TNF标准上一页 [1] [2] [3] 下一页
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