Silicosis is characterized by pulmonary fibrosis due to long-term inhalation of silica particles. Although the cause of this serious disease is known, its pathogenesis remains unclear and there are currently no specific treatments. Recent studies have shown that the anti-oxidant transcription factor Nrf2 is expressed at reduced levels in fibrotic foci, which may be related to disease progression. However, the molecular mechanisms by which this might occur have yet to be elucidated. Sodium tanshinone IIA sulfonate (STS), an extract of Salvia miltiorrhiza, is used in traditional Chinese medicine in the treatment of coronary heart disease. STS has been shown to play a strong anti-oxidative role in various organs. Here, we employed a rat model to explore the effects of STS on oxidative stress and the progression of fibrosis in silicosis. STS significantly reduced collagen deposition in the lungs, thereby antagonising silicosis. Immunohistochemical and immunofluorescence staining showed that Nrf2 was differentially expressed in lung cells during silica induced fibrosis, and chromatin immunoprecipitation-sequencing experiments demonstrated that Nrf2 promoted the expression of the antioxidant proteins thioredoxin and thioredoxin reductase. Our results suggest that the anti-fibrotic effects of STS may be related to upregulation of Nrf2 nuclear expression, especially in fibrotic lesions, and the promotion of thioredoxin and thioredoxin reductase expression. Our findings may open up new avenues for the development of STS as a treatment for silicosis.

矽肺病的特征是由于长期吸入二氧化硅颗粒而导致的肺纤维化。尽管已知这种严重疾病的病因，但其发病机理仍不清楚，目前尚无特异性治疗方法。最近的研究表明，抗氧化转录因子Nrf2在纤维化灶中的表达水平降低，这可能与疾病的进展有关。然而，可能发生这种情况的分子机制尚未阐明。丹参提取物丹参酮IIA磺酸钠（STS）被用于中药治疗冠心病。STS已显示在各种器官中起着强大的抗氧化作用。在这里，我们采用了大鼠模型来探讨STS对矽肺病中氧化应激和纤维化进程的影响。STS显着减少了肺中胶原蛋白的沉积，从而拮抗了矽肺病。免疫组织化学和免疫荧光染色显示，Nrf2在二氧化硅诱导的纤维化过程中在肺细胞中差异表达，染色质免疫沉淀测序实验表明Nrf2促进了抗氧化蛋白硫氧还蛋白和硫氧还蛋白还原酶的表达。我们的结果表明，STS的抗纤维化作用可能与Nrf2核表达的上调，尤其是在纤维化病变中，以及硫氧还蛋白和硫氧还蛋白还原酶表达的促进有关。我们的发现可能为STS的发展为矽肺病的治疗开辟新的途径。免疫组织化学和免疫荧光染色显示，Nrf2在二氧化硅诱导的纤维化过程中在肺细胞中差异表达，染色质免疫沉淀测序实验表明Nrf2促进了抗氧化蛋白硫氧还蛋白和硫氧还蛋白还原酶的表达。我们的结果表明，STS的抗纤维化作用可能与Nrf2核表达的上调，尤其是在纤维化病变中，以及硫氧还蛋白和硫氧还蛋白还原酶表达的促进有关。我们的发现可能为STS的发展为矽肺病的治疗开辟新的途径。免疫组织化学和免疫荧光染色显示，Nrf2在二氧化硅诱导的纤维化过程中在肺细胞中差异表达，染色质免疫沉淀测序实验表明Nrf2促进了抗氧化蛋白硫氧还蛋白和硫氧还蛋白还原酶的表达。我们的结果表明，STS的抗纤维化作用可能与Nrf2核表达的上调，尤其是在纤维化病变中，以及硫氧还蛋白和硫氧还蛋白还原酶表达的促进有关。我们的发现可能为STS的发展为矽肺病的治疗开辟新的途径。染色质免疫沉淀测序实验表明，Nrf2促进了抗氧化蛋白硫氧还蛋白和硫氧还蛋白还原酶的表达。我们的结果表明，STS的抗纤维化作用可能与Nrf2核表达的上调有关，尤其是在纤维化病变中，以及硫氧还蛋白和硫氧还蛋白还原酶表达的促进。我们的发现可能为STS的发展为矽肺病的治疗开辟新的途径。染色质免疫沉淀测序实验表明，Nrf2促进了抗氧化蛋白硫氧还蛋白和硫氧还蛋白还原酶的表达。我们的结果表明，STS的抗纤维化作用可能与Nrf2核表达的上调，尤其是在纤维化病变中，以及硫氧还蛋白和硫氧还蛋白还原酶表达的促进有关。我们的发现可能为STS的发展为矽肺病的治疗开辟新的途径。