〔Abstract〕 Objective To investigate the expression of class A scavenger receptor 1(MSR1) in the lungs of silicosis mice and its role in inflammation and lipid metabolism mediated by mouse mononuclear macrophages(RAW264.7). Methods 24 C57BL/6 male mice were randomly divided into control group, exposed 7 d group, exposed 14 d group, exposed 28 d group, with 6 mice in each group. RAW264.7 cells were divided into control group, siRNA-MSR1 group, SiO2group and siRNA-MSR1+SiO2stimulation group. The pathological changes of lung tissue in mice were observed by HE and VG staining. Lipid accumulation was observed under oil red O staining microscope. Immunohistochemical staining(IHC) was used to detect the expression and localization of MSR1. The expression of MSR1, tumor necrosis factor(TNF)-α, interleukin(IL)-6 and IL-1β were detected by Western blot. Results Compared with the control group, HE and VG staining results showed that inflammatory cells gathered and collagen distribution increased in the lung tissue of silicosis mice. Oil red O staining showed that a large number of orange-red lipid droplets appeared in the lung tissue of mice. IHC results showed that the expression of MSR1 was up-regulated in silicosis inflammation stage. Western blot results showed that the expression of MSR1, TNF-α, IL-6 and IL-1β was up-regulated in silicosis inflammation stage(P<0.05). The expression of MSR1 in the SiO2cell stimulation group was up-regulated(P<0.05), and the expression of MSR1 in the siRNA-MSR1 group decreased(P<0.05), and lipid droplets also appeared in the SiO2cell stimulation group. The accumulation of lipid droplets in siRNA-MSR1+SiO2stimulation group was lower than that in SiO2group(P<0.01). ELISA results showed that the expression of TNF-α, IL-6 and IL-1β in SiO2cell stimulation group was up-regulated(P<0.05). Compared with SiO2group, the expression of TNF-α, IL-6 and IL-1β in siRNA-MSR1+SiO2stimulation group was down-regulated(P<0.05). Conclusion MSR1 is involved in the regulation of lipid components and the release of inflammatory factors in lung tissue and cells of silicosis mice. Inhibition of MSR1 expression can antagonize the inflammatory response and abnormal lipid accumulation in macrophages. MSR1 may be a potential therapeutic target for future intervention in the progression of silicosis.