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矽肺发病机理研究 被引量:6

Study on the Mechanism of Silicosis and a New Drug for Silicosis
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摘要 石英(SiO2)进入肺中首先被AM吞噬。石英损伤巨噬细胞,导致细胞的氧化代谢下降,并导致释放一些生物活性物质,对细胞有毒性作用,或能促进成纤维细胞增生与胶原台成,有的还可抑制腔原合成。通过获取支气管肺泡冲洗液(BALF),可以得到肺泡巨噬细胞及其分泌物。本课题中进行,以下的几项检查。 In this study, the biological changes insilicosis were studied systematically. First the changes in bronchoalveolar fluidwere observed including the determination oflysozyme, total proteins, interleukin-1, fibro-nectin, ceruloplasmin, lipids and the metabo-lic activity of cells. It was proved that thechanges of the above mentioned substanceswere obviously correlated with the develop-ment of silicotic lesion in the lung. Second, contents of main components insilicotic nodules including collagen, proteogl-ycan and lipids were found not only increas-ed abnormally in quantities, but also changedin composition, for example, ratio of collagentype Ⅰ/Ⅲ was higher than normal lung colla-gen. Levels of other components, such asceruloplasmin, fibronectin, prostaglandin E andlipid peroxides were also increased which de-noted that they were all closely related withthe formation of silicotic fibrosis. Infraredspectrophotographic analysis proved that SiO_2presented in the silicotic nodules in the formof -Si-O-R-, may be reacted as a cross link-ing bridge. between collagen fibers. Third, a protein was isolated from me-dium of silicaingested macrophages. Its bioch-emical properties were characterized. Resultsof Western Blot methods proved that it com-bined with antibody of ceruloplasmin.It alsoshowed strong activity in stimulating the syn-thesis of collagen. A new drug called Xinin was discovered.It showed good effect and low toxicity to ex-perimental silicotic animals, such as rats anddogs. The pharmacological studies were perfur-triamed and the drug was ready for clinicaltrials.
作者 李玉瑞
出处 《中国工业医学杂志》 CAS 1991年第2期20-23,共4页 Chinese Journal of Industrial Medicine
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