Résumé
Objective To explore the role and mechanism of tumor necrosis factor ligand -related molecule 1A (TL1A) in chronic experimental colitis associated intestinal fibrosis .Methods The model of chronic experimental colitis-associated intestinal fibrosis was induced by dextran sodium sulfate (DSS).The mice with high TL1A (L-Tg) expression in lymphoid cells and wild -type mice with the same genetic background were divided into wild type control group, wild type DSS group, transgenic control group and transgenic DSS group.The changes of body mass, length of colon, disease activity index (DAI) and colonic pathological score were compared among different groups .The degree of colonic inflammation was evaluated by Hematoxylin -Eosin (H-E) staining.The degree of intestinal fibrosis was assessed by Masson staining and Sirius red staining .The expression of vimentin, αsmooth muscle actin ( α-SMA), type Ⅰ collagen, Ⅲ collagen and transforming growth factor-β1 ( TGF-β1 ) /Smad3 in colon tissue was examined by immunohistochemistry .T test was performed for statistical analysis.Results The body mass of the transgenic DSS group decreased by (9.6 ± 1.8)％, which was more than wild-type DSS group (6.2 ±1.3)％, the difference was statistically significant (t =3.751, P <0.01).The DAI score and colonic pathological score of transgenic DSS group were both higher than those of wild-type DSS group (7.33 ±0.58 vs.6.00 ±1.00, and 14.00 ±1.05 vs.11.75 ±0.50, respectively), and the differences were statistically significant (t =2.818 and 4.739, both P <0.05).The results of Masson staining and Sirius red staining showed aggravation of intestinal fibrosis .The results of immunohistochemical staining showed that the cumulative positive absorbance values of vimentin , α-SMA, TGF-β1 and Smad3 of wild-type DSS group were lower than those of transgenic DSS group (0.650 ±0.050 vs. 0.800 ±0.020, 0.390 ±0.040 vs.0.600 ±0.040, 0.550 ±0.040 vs.0.730 ±0.040, 0.590 ±0.020 vs. 0.830 ±0.040), and the differences were statistically significant (t =6.823, 9.093, 7.794 and 10.390, all P <0.01).Conclusion TL1A may promote the proliferation and activation of fibroblasts through TGF -β1 /Smad3 pathway, leading to the genesis and development of experimental colitis associated intestinal fibrosis .
Résumé
Objective To explore the expression of tumor necrosis factor(TNF) ligand-related molecule-1A(TL1A) in mice with viral myocarditis(VM) and the role of astragaloside.Methods Fifty-five male Balb/c mice were randomly divided into 4 groups:control group,model group,low-dose intervention group and high-dose intervention group.Mice in model group,low-dose intervention group and high-dose intervention group were inoculated with 0.1 mL coxsackie B3 virus intraperitoneally.Then,mice in low-dose intervention group and high-dose intervention group were treated with 10 g?L-1 and 90 g?L-1 astragaloside solution,respectively.Mice in control group and model group were treated with 0.1 mL carboxymethycellulose solution.All mice were killed on the 15thday.Histological cross sections of heart were stained with hematoxylin-eosin and myocardial histopathologic scores were counted under optical microscope.The expressions of myocardial TL1A mRNA and protein were detected by reverse transcription polymerase chain reaction and immunohistochemistry.Results The mortality were 0,46.7%,40.0% and 13.3% in control group,model group,low-dose intervention group and high-dose intervention group,respectively.Compared with model group and low-dose intervention group,the mortality was significantly lower in high-dose intervention group(?2=9.46,8.95,Pa