ABSTRACT
Objective To explore the effect of rapamycin on pulmonary fibrosis in rats and its mechanism.Methods Pulmonary fibrosis model was induced by intratracheal instillation of bleomycin (5mg/kg).Control group was treated by intratracheal instillation of saline (1.25 ml/kg) to obtain the negative control.The rats of the rapamycin-treated group were given rapamycin (1 mg/kg per day) by gastric perfusion for consecutive 10 days beginning on the third day after intratracheal instillation of bleomycin.On the 28th day,all rats were sacrificed and the peripheral blood and the lung tissues were harvested.Lung tissues were performed hematoxylin-eosin (HE) staining.The severity of pulmonary fibrosis in rats was assessed by Ashcroft score.Lung tissues were performed immunohistochemical staining to detect the expression of transforming growth factor beta (TGF-beta).The expression level was judged by integrated optical density.Results The severity of pulmonary fibrosis was improved in rats of rapamycin-treated group compared with the rats of bleomycin-treated group.A significant difference in Ashcroft score was found between rapamycin-treated group and bleomycin-treated group(2.92 ± 0.64 vs 5.76 ± 1.76,P ＜ 0.01).The expression level of TGF-β was increased in rapamycin-treated group compared with the normal control group (5520.00 ± 1614.20 vs 3370.00 ± 1478.14,P ＜0.01).The expression level of TGF-β was decreased in rapamycin-treated group compared with the bleomycin-treated group (5520.00 ± 1614.20 vs 7772.00 ±1526.46 P ＜0.01).Conclusions Rapamycin can prevent bleomycin-induced pulmonary fibrosis.
ABSTRACT
ObjectiveTo observe the effect of rapamycin on the proliferation and cell cycle of prostate cancer cell lines PC3,and to investigate the mechanism that it inhibits the growth and metastasis of prostate cancer cells.MethodsPC3 cells were cultured in vitro,and treated with different concentrations (10,25ng/ml) of cycle raparnycine.MTT was used to measure the change of proliferation of PC3 cells.Flow cytometry was used to measure the changes of cell cycle and apoptosis of PC3 cells.Nude mice were used to detect the effect of rapamycin on metastasis.ResultsThe proliferation of PC3 cells was significantly inhibited by rapamycin,and a time- and concentration-dependent relationship was shown,the inhibited rate was(42.23 ± 0.78 ) ％ after 36 h in the group of 25 ng/ml ( P ＜ 0.05 ).Flow cytometry analysis showed rapamycin significantly inhibited the cell cycle,prompted the apoptosis,and increased the number of cells in G0/G1 phase at 36 h with a rate of cell staying at Go/G1 [ (92.17 ± 0.69 ) ％ ] ( P ＜ 0.05 ).The weight of tumors in nude mice in the control group was significantly greater than that in RPM group[ (3.41± 0.28)g vs ( 1.19 ± 0.23 )g] ( P＜ 0.05 ),and metastatic sites of the lung and liver in the control group were significantly mote than the RPM group [ 100％ (7/7) vs 14.29％ ( 1/7 ) ] ( P ＜ 0.05 ).Conclusions Rapamycin significantly inhibits the proliferation and metastasis of osteosarcoma.The rapamycin-based regimen is valuable for clinical application.