中文摘要：

目的研究煤工尘肺患者血清中溶血磷脂酸（LPA）、血管内皮生长因子（VEGF）、内皮素（ET）水平与煤尘接触所致肺纤维化的关系，探讨LPA、VEGF和ET在煤工尘肺肺纤维化发生中的作用。方法选取诊断为煤工尘肺患者62例作为煤工尘肺组，其中I期23例，Ⅱ期25例，Ⅲ期14例；选取有2年以上职业性煤尘接触史但未诊断为尘肺的职业健康体检者20例作为接尘组；无职业性粉尘接触史的健康体检者10例作为对照组。应用酶联免疫吸附方法测量血清中LPA、VEGF和ET的浓度。结果与健康对照组比较，接尘组和各期煤工尘肺组血清中VEGF、ET含量明显升高，差异有统计学意义（P〈0．05）；接尘组、Ⅰ期和Ⅱ期煤工尘肺组血清LPA明显高于健康对照组，差异有统计学意义（P〈0．05）。接尘组和各期煤工尘肺组血清LPA与VEGF、ET水平有明显正相关关系（P〈0．05）。LPA与VEGF和ET的相关系数R值：接尘组中LPA与VEGF和ET的相关系数分别为0．707、0．891（P〈0．05，P〈0．01），Ⅰ期煤工尘肺组LPA与VEGF和ET的相关系数分别为0．955、0．980（P〈0．01，P〈0．01），Ⅱ期煤工尘肺组LPA与VEGF和ET的相关系数分别为0．946、0．958（P〈0．01，P〈0．01），Ⅲ期煤工尘肺组LPA与VEGF和ET的相关系数分别为0．961、0．954（P〈0．01，P〈0．01）。结论肺部新生血管形成可能参与了煤工尘肺肺纤维化的发生和发展，对于探索尘肺病发病机制和早期治疗提供了理论依据。

英文摘要：

Objective To explore the role of lysophosphatidic acid, vascular endothelial growth facor and endothelin in the pathogenesis of pulmonary fibrosis in coal workers＇ pneumoconiosis patients, the relationship of lysophosphatidic acid, VEGF and ET in serum was studied. Methods Sixty two pneumoconiosis patients were selected as cases group, which included 23 cases of stage Ⅰ , 25 cases of stage Ⅱ and 14 cases of stageⅢ. Twenty workers were selected as dust exposure group who exposed to coal dust for more than 2 years and had not been diagnosed as pneumoconiosis. Ten healthy people who had no occupational dust exposure were simultaneously selected as the control group. The serum levels of LPA, VEGF and ET were measured by ELISA. Results The serum levels of VEGF and ET in coal dust exposed group and pneumoconiosis group were much higher than in the control group. The differences were statistically significant among the three groups （P〈0.01）. The serum levels of LPA increased in the dust exposed group, stage Ⅰ and stage Ⅱ group. The serum levels of LPA correlated positively with the levels of VEGF and ET（P〈0.05）. Conclusions The serum levels of LPA, VEGF and ET had evident correlation with the pulmonary fibrosis caused by coal dust, which indicate that LPA, VEGF and ET may play a pivotal role in the process of pulmonary fibrosis. The study will throw light on both pathogenesis and early intervention for pneumoconiosis.