RESUMO
Aim To explore the protective effects of in-terleukin-17 ( IL-17 ) monoclonal antibody ( mAb ) on bleomycin-induced pulmonary fibrosis rats and the re-lated mechanisms. Methods Seventy-five male SD rats were randomly divided into normal control group, sham operation group, model group, non-specific IgG group and IL-17 mAb group. Each group included fif-teen rats. Rats in the latter three groups were intratra-cheally administered with bleomycin A5 to establish pulmonary fibrosis model, whereas the ones in sham operation group were treated with the same volume of physiological saline. On day 7, 14 and 21, rats in non-specific IgG group and IL-17 mAb group were in-jected with non-specific IgG and IL-17 mAb, respec-tively,through the caudal vein. However,the ones in the other groups were administered with the same volume of physiological saline. All rats were sacrificed on day 28. Pulmonary tissues were then removed, and HE and Masson staining was performed. The contents of IL-17, IL-6 and tumor necrosis factor-α ( TNF-α) in pulmo-nary tissues were measured by enzyme linked immu-nosorbent assay ( ELISA ) . Western blot was used to analyze the pulmonary tissues protein expression of nu-clear factor-κB ( NF-κB) p65 in the nucleus as well as collagen type I ( Col Ⅰ) and collagen type III ( ColⅢ) in the whole cells. The levels of Col Ⅰ and ColⅢ in the pulmonary tissues were detected by fluores-cence real-time quantitative PCR. Serum was separa-ted, and the concentrations of procollagen type 1 carboxyterminal propeptide ( PICP ) and procollagen type III aminoterminal propeptide ( PIIINP ) in serum were then measured by ELISA. Results The severity of alveolitis and pulmonary fibrosis was lower in IL-17 mAb group than that in model group and non-specific IgG group ( P 0. 05 ) . Similar results were also seen between sham operation group and normal control group ( P >0. 05 ) . Conclusion IL-17 mAb protects rats from pulmonary fibrosis by inhibiting inflammatory response via downregulating NF-κB expression and decreasing collagen synthesis in the pulmonary tissues.
RESUMO
Aim To explore the inhibitory effects of resveratrol (Res ) on human pulmonary fibroblast growth,and its related mechanisms.Methods Hu-man pulmonary fibroblasts MRC-5 were cultured in vitro as research object.These cells were inoculated with 20 μL dimethyl sulfoxide (DMSO)as well as 0, 12.5,25 50,100 and 200 μmol·L-1 Res for 24,48 and 72 h,respectively.Inhibitory rate of cellular pro-liferation was analyzed by MTT.In addition,these cells were treated with 20 μL DMSO (medium group) as well as 50 and 100 μmol·L-1 Res for 48 h,re-spectively.Subsequently,cell cycle and apoptotic rate were measured using flow cytometry.Apoptosis index (AI ) was detected through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). The mRNA and protein expression of cell cycle protein D1 (Cyclin D1 ) and cyclin-dependent kinase 4 (CDK4)was detected through fluorescence real-time quantitative PCR and Western blot, respectively. Western blot was used to measure the protein expres-sion of Bcl-2 and Bax.Results With the increase of Res concentrations and prolongation of treated time, inhibitory rate of cellular proliferation was gradually el-evated (P<0.01).After 48 h of co-culture,DNA ra-tio of S and G2/M periods,mRNA and protein levels of Cyclin D1 and CDK4,and Bcl-2 protein levels were significantly decreased while DNA ratio of G0/G1 peri-od,AI,apoptotic rate and Bax protein levels were sig-nificantly increased in 50 and 100 μmol · L-1 Res-treated groups as compared to medium group (P <0.01 ).Moreover,the effects 100 μmol · L-1 Res were better than those of 50 μmol · L-1 Res (P <0.01).Conclusion Res can suppress the prolifera-tion of MRC-5 cells,which may be associated with blockade of cell cycle progression and induction of cell apoptosis.