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Objective To study the influence of theaflavin on the expressions of TLR4 and release of TNF-αand IL-6 in primari-ly cultured rat airway epithelial cells .Methods Lipopolysacchride(LPS) was adopted to establish the in vitro inflammatory injury model of rat airway epithelial cell ,the TNF-αand IL-6 secreted by the airway epithelial cells and the TLR4 protein level in the air-way epithelial cells were detected with ELISA and the expressions of TLR4 mRNA was detected with RT-PCR .Results LPS sig-nificantly induced the airway epithelial cells to secrete TNF-αand IL-6 ,and enhanced the TLR4 mRNA and TLR4 protein expres-sion(P<0 .01) .Theaflavin could inhibit LPS induced TNF-αand IL-6 secretion and TLR4 gene expression(P<0 .05) ,which was related with the theaflavin concentration (P<0 .05) .Conclusion In rat airway epithelial cell culture ,the anti-inflammatory effect of theaflavin may be decrease the release of inflammatory cytokines via inhibiting TLR 4 gene expression and LPS/TLR4 signal trans-duction pathway .
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Objective: To investigate the effect of tumor necrosis factor-α converting enzyme (TACE) on mucous hypersecretion in inlf ammatory airway. Methods: Mucous hypersecretion model of human lung adenocarcinoma cells A549 was induced by human neutrophil elastase (HNE), and TNF-α converting enzyme inhibitor-1 (TAPI-1), an inhibitor of TACE, was chosen for the inference study. The expression of MUC5AC and TACE was examined. hT e cells were divided into 5 groups: a negative control group, HNE1 (15 nmol/L) group, HNE2 (25 nmol/L) group, HNE3 (50 nmol/L) group and TAPI-1 group. RT-PCR was used to examine MUC5AC and TACE mRNA expression. The protein expression of TACE and MUC5AC was examined by Western blot and ELISA, respectively. Results: HNE induced the TACE and MUC5AC mRNA and protein expression in a dose-dependent manner. Compared with the control group, the increases were all signiifcantly increased in the three dosages of HNE group (P<0.01). The HNE-induced TACE and MUC5AC mRNA and protein expression were dramatically attenuated in the presence of TAPI-1, an inhibitor of TACE (P<0.01). Conclusion: TACE participated cell signalling pathway of airway mucous hypersecretion, and could down regulation the level of inlfammation airway mucous hypersecretion.
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OBJECTIVE@#To determine the relation between serum myostatin with body mass index (BMI) and PaO₂/PaCO₂ in men with chronic obstructive pulmonary disease (COPD).@*METHODS@#A cohort of outpatients with stable COPD was evaluated. We evaluated the myostatin, PaO₂/PaCO₂ and BMI, and the patients were stratified by BMI. The plasma level of myostatin and PaO₂/PaCO₂ was measured by high sensitivity ELISA or blood gas analysis.@*RESULTS@#PaCO₂ and myostatin increased significantly compared with those in the control group (P<0.05), but PaO₂ decreased significantly. There was positive correlation between myostatin and PaCO₂ (P<0.05), and negative correlation between myostatin and BMI/FEV1/pred value/PaO₂ (P<0.05).@*CONCLUSION@#Patients with higher myostatin levels had a lower BMI, lower PaO₂ and higher PaCO₂, with poor pathogenetic condition and prognosis. Myostatin may be a potential treatment target in patients with chronic obstructive pulmonary disease.