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.

Disease Progression ; Hepatic Stellate Cells ; Hepatitis B, Chronic ; Humans ; Liver Cirrhosis ; Receptors, Cannabinoid

BACKGROUNDIt was reported that tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) was a powerful pulmonary carcinogen, predominantly inducing adenocarcinoma of the lung in mouse. The aim of this study is to assay metabolites of NNK, which are 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its O-glucuronide (NNAL-Gluc), and their ratio (NNAL-Gluc/NNAL) in smokers and non-smokers' urine, and to explore the carcinogenicity of NNK among different people.

METHODSUsing high pressure liquid chromatograph (HPLC) and gas chromatograph-mass tadom (GC-MS/MS), NNAL-Gluc and NNAL in 24h urine were detected in 8 healthy smokers, 10 lung cancer smokers and 4 healthy non-smokers.

RESULTSBoth of the two metabolites were not found in non-smokers' urine. The ratios of urine NNAL-Gluc/NNAL were greatly different among different smokers. The mean ratio of NNAL-Gluc/NNAL in healthy smokers was 4.95, and 0.5 in lung cancer smokers.

CONCLUSIONSThe results provide the first evidence for metabolite detection of tobacco-specific nitrosamine in Chinese smokers' urine . The result suggests that detoxification ability of healthy smokers is higher than that of lung cancer smokers. It may provide a detective way to screen high risk people for lung cancer in smokers.

80%). The resulting bulk cultures were mainly comprised of a CD56~- subset of ??T cells. The expression of V?1, V?2 and V?3 gene families in the ex vivo multiplied ??T cells from TIL and PBMC of patients with NPC, and PBMC of normal control was demonstrated by RT-PCR. Conclusion The ??TIL of NPC can be multiplied in vitro for the first time. The subsets (V?1, V?2 and V?3) of ??T cells from PBMC of healthy individuals, PBMC and TIL of patients with NPC, can also be multiplied in vitro, and the experiment lays an experimental foundation of using ??T cells for the cellular adoptive therapy in patients with NPC.