RESUMEN
Objective:To explore the effects of Silybin on pulmonary inflammatory injury and macrophage apoptosis in pulmo-nary tuberculosis(TB)rats,and its regulation on death receptor Fas and its ligand FasL.Methods:TB rat model was prepared by tail vein injection of Mycobacterium tuberculosis(Mtb).Rats were randomly separated into model group,Silybin group,Fas overexpres-sion recombinant protein(pcDNA-Fas)group,pcDNA-Fas negative control(pcDNA-NC)group and Silybin+pcDNA-Fas group,with 15 rats in each group,and another 15 rats were selected as normal control group.Acid-fast staining was used to measure infection of lung tissue;HE staining was performed to observe pathological changes of lung tissue;expressions of TNF-α and IL-6 in lung tissue were detected by ELISA;apoptosis rate of alveolar macrophages was detected by flow cytometry combined with Annexin V-FITC/PI staining;expression levels of Fas,FasL,caspase8,caspase3 and macrophage inflammatory protein-2(MIP-2)were detected by Western blot.Results:Compared with normal control group,expressions of inflammatory factors in lung tissue and apoptotic rate of alveolar macrophages were increased in model group,Mtb infection and caseous necrosis in lung tissue were severe,and Fas/FasL-mediated caspase8/3 apoptotic pathway was activated(P<0.05).Compared with model group,expressions of inflammatory factors in lung tissue and apoptosis rate of alveolar macrophages in Silybin group were reduced,Mtb infection and caseous necrosis in lung tissue were alleviated,and the activity of Fas/FasL-mediated caspase8/3 apoptosis pathway decreased(P<0.05).pcDNA-Fas was able to further activate Fas/FasL-mediated caspase8/3 apoptotic pathway,aggravate lung tissue Mtb infection and caseous necrosis,promote inflammatory damage in lung tissue and macrophage apoptosis,and weaken the anti-Fas/FasL activation,anti-inflammatory and anti-apoptotic effects of Silybin(P<0.05).Conclusion:Silybin may play an anti-Mtb infection,anti-apoptosis of lung tissue macro-phages and anti-inflammatory effects by inhibiting the Fas/FasL signaling pathway.