Objective To study the protective effect and mechanism of adenosine A2a receptor(A2aR)activation in the pathogenesis of systemic sclerosis associated interstitial lung disease(SSc-ILD).Methods A total of 24 healthy female Balb/c mice were randomly divided into three groups:wild normal control(WN)group,wild model(WM)group,WM with CGS21680(WMC)group.Two weeks after the end of injections,the lung samples and serum of mice were collected.A part of lung tissues were obtained for hematoxylin eosinstaining,Masson staining and determination of hydroxyprolineto observe the degree of inflammation and fibrosis.Enzyme linked immunosorbent assay(ELISA)was used to detect advanced oxidative protein products in mouse serum and lung tissue,reduced glutathione in lung tissue,and oxidative stress levels in serum and lung tissue.Results①Underhematoxylin eosinstaining and Masson staining,the lungs of mice in WM group showed inflammation infiltration and fibrosis,while mice in WMC group showed a reduction compared to mice in WM group;②The content of hydroxyproline in lung tissue,serum and late stage oxidative protein products in lung tissue of WM group mice increased compared to WN group mice(P<0.01),while the content of WMC group mice decreased compared to WM group mice(P<0.01);③The reduced glutathione content in lung tissue of WM group mice was lower than that of WN group mice(P<0.01),while WMC group mice were higher than WM group mice(P<0.05).Conclusion The activation of A2aR ameliorated the degree of inflammation and fibrosis in SSc-ILD,possibly through the antioxidant mechanism.