RESUMO
OBJECTIVE To investigate the inhibitory effects of formononetin on lipopolysaccharide （LPS）-induced apoptosis and inflammatory response in alveolar epithelial cells through phosphoinositide 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway. METHODS Human lung cancer alveolar basal epithelial cells A549 were cultured in vitro and divided into control group （no intervention）， model group （1 μg/mL LPS）， different concentrations of formononetin groups （1 μg/mL LPS+6.25， 12.5， 25， 50 μmol/L formononetin）. The levels of inflammatory factors （interleukin-8， tumor necrosis factor-α） and cell viability were detected in each group. Another A549 cells were divided into control group， model group （1 μg/mL LPS）， LPS+25 group （1 μg/mL LPS+25 μmol/L formononetin）， inhibitor group （1 μg/mL LPS+20 μmol/L LY294002）， formononetin+inhibitor group （1 μg/mL LPS+25 μmol/L formononetin+20 μmol/L LY294002） and formononetin+activator group （1 μg/mL LPS+25 μmol/L formononetin+ 10 μmol/L SC79）. The secretion levels and mRNA expressions of inflammatory factors， cell apoptosis， and expressions of the key proteins of PI3K/Akt signaling pathway were detected in each group. RESULTS Compared with model group， the levels of inflammatory factors were decreased significantly after the intervention of 25 μmol/L of formononetin， and the cell viability was increased significantly （P＜0.05）. Compared with the control group， the secretion levels and mRNA expressions of inflammatory factors， apoptotic rate， and relative expressions of phosphorylated Akt and phosphorylated PI3K of the model group were increased significantly （P＜0.05）. Compared with the model group， the above indexes of the LPS+25 group and the inhibitor group were decreased significantly （P＜0.05）. Compared with the LPS+25 group， the above indicators of formononetin+inhibitor group were further decreased， while those of formononetin+activator group were increased significantly （P＜0.05）. CONCLUSIONS Formononetin can inhibit LPS-induced epithelial cell apoptosis and improve inflammatory response， and the mechanism may be related to the inhibition of the PI3K/Akt signaling pathway.
RESUMO
Objective To explore the relapse rate of the patients with primary smear-positive pulmonary tu-berculosis and pyrazinamide-resistance. Methods Retrospective analysis was made on the relapse for 150 patients with primary smear-positive pulmonary tuberculosis , who had been diagnosed and completed treatment in Guangzhou Chest Hospital from January 2012 to August 2013 , and had followed up two years. According to the re-sults of drug susceptibility test before treatment, they were divided into pyrazinamide-sensitive (114 cases) and pyrazinamide-resistant (36 cases) groups. Results (1)By the end of the treatment, the recovery rates in the sensi-tive group and resistant group were 98.25%and 88.89%respectively (P=0.044). The rate of the lesions absorption was 99.12%and 94.44%respectively (P=0.143). The rate of the cavity shrinking was 89.01% and 70.37% re-spectively (P = 0.039). The rate of the relapse was 3.57% and 6.25% respectively (P = 0.867) within 2 years fol-low-up in the sensitive group and the resistant group. Conclusions PZA has certain effects on the patients with primary smear-positive pulmonary tuberculosis. Those who are tolerant would have lower incidence for cavity shrink-ing. But the relapse rate for two-year follow-up showed there were not significant differences in two groups.