Objective To explore the role of miR-204-3p in silicosis and to elucidate the mechanism by which it affects silicosis fibers by regulating silica dust-induced alveolar epithelial-mesenchymal transition (EMT) in rats. Methods Forty SD rats were divided randomly into 4 groups: Control, Silicosis, AAV-Control, and AAV-miR-204-3p groups. The pathology of lung tissue damage was detected by hematoxylin and eosin ( HE) and Masson staining. Relative expression levels of miR-204-3p and EMT marker genes in lung tissues from rats in each group were analyzed by real-time fluorescence reverse transcription quantitative PCR(RT-qPCR), and protein expression levels of EMT-related markers in lung tissues were detected by Western blot. Results The alveolar structure was damaged,the lung septa showed interstitial fibrosis, and expression levels of mesenchymal markers were elevated in the Silicosis group compared with the Control group (P<0. 05, P<0. 01, P<0. 001). The alveolar structure was more complete,the EMT process was alleviated, fibrosis was improved, and mesenchymal marker expression was reduced in the AAVmiR-204-3p group compared with the AAV-Control group (P<0. 05, P<0. 01, P<0. 001). Conclusions Free silica dust induces EMT in rat lung tissue. Overexpression of miR-204-3p can attenuate the EMT process induced by free silica dust in rats, and may thus affect silicosis fibrosis.