Objective To investigate the effect of diammonium glycyrrhizinate(DG)on pulmonary injury of rats with pulmonary tuberculosis.Methods The rat models of pulmonary tuberculosis were constructed and then the an-imals were randomly divided into model group,diammonium glycyrrhizinate treatment groups(low-dose,medium-dose and high-dose)groups,high dose of diammonium glycyrrhizinate plus peroxisome proliferator-activated receptor γ(PPARγ)inhibitor group(H-DG+GW9662 group),and another 18 rats were selected as control group.The colony count of Mycobacterium tuberculosis(Mtb)in lung tissue was detected.HE staining microscopy was ap-plied to detect lung histopathology.TUNEL was applied to detect apoptosis of lung tissue cells.ELISA was applied to detect serum level of inflammatory factors.Western blot was applied to measure PPARγ,phosphorylated p38 mi-togen-activated protein kinase(p-p38MAPK)and p38 mitogen-activated protein kinase(p38MAPK)in lung tissue.Results Compared with the control group,the lung tissue structure in model group was severely damaged with a large number of proliferative tuberculosis nodules,changes of alveolar morphology,inflammatory cell infiltration and even caseous necrosis were found,and the number of tuberculosis colonies,apoptosis rate,TNF-α,IL-6,IFN-γ,COX-2 levels,and p-p38MAPK/p38MAPK expression were all increased,while PPARγ expression was decreased(P＜0.05).In L-DG,M-DG,H-DG groups improvement of lung tissue structure,alveolar morphology,inflammatory cell infiltration,and caseous necrosis were found as compared to the model group,while the counting number of tuberculosis colonies decreased and rate of cell apoptosis decreased.The level of TNF-α,IL-6,IFN-γ,COX-2 and expression of p-p38MAPK/p38MAPK reduced,the expression of PPARγ all increased.The H-DG group showed the most significant changes(P＜0.05).GW9662 treatment significantly reversed the improvement of DG on pulmonary injury in rats with pulmonary tuberculosis.Conclusions DG improves lung injury in rats with pul-monary tuberculosis and its mechanism is potentially related to the activation of PPARγ pathway and inhibition of p38MAPK pathway.