RESUMEN
Objective: To investigate the effects of dexamethasone on transforming growth factor [TGF]-beta1/Smads signaling pathway in benign biliary stricture [BBS] fibroblasts
Study Design: An experimental study
Place and Duration of Study: Guizhou Medical University, Guiyang, Guizhou, China, from January to August 2016
Methodology: Fibroblasts derived from rabbit BBS model were cultured and identified, then treated by different concentration of dexamethasone [0.02, 0.1 and 0.5 mg/ml]. Dexamethasone-treated cells and non-treated control groups were incubated respectively for 48 hours. Cell proliferation was assessed using cell counting kit-8. Relative mRNA expression of TGF-beta1, Smad4 and Smad7 were assessed by quantitative RT-PCR. Protein expression of TGF-beta1 and Smad4 were investigated by Western blotting
Results: Treatment with dexamethasone significantly inhibited the proliferation of BBS fibroblasts, significantly attenuated both the mRNA and protein expression of TGF-beta1 and Smad4, and significantly up-regulated the mRNA expression of Smad7 in BBS fibroblasts [all p<0.05, 0.1-0.5 mg/ml], and exhibited in a dose-dependent manner
Conclusion: TGF-beta1/Smads signaling pathway may play an important role in BBS progression; dexamethasone significantly altered the expression of TGF-beta1/Smads signaling pathway and significantly inhibited cell proliferation in rabbit BBS fibroblasts. Therefore, dexamethasone may be a therapeutic option for the prevention of BBS
RESUMEN
Objective: To investigate the effects of tetramethylpyrazine [TMP] on transforming growth factor-beta1 [TGF- beta1], alpha-smooth muscle actin [alpha-SMA], and neuronal regeneration related protein [P311] in benign biliary stricture fibroblasts of rabbit. Study Design: An experimental study. Place and Duration of Study: Guizhou Medical University, Guiyang, Guizhou, China, from April to December 2015
Methodology: Fibroblasts isolated from rabbits following benign biliary stricture were cultured and treated with different concentrations of TMF [0.08, 0.4. and 2.0 mg/ml]. TMP-treated cells and non-treated control groups were incubated for 48-hours, and proliferation was assessed using the cell counting kit-8 assay. The mRNA expressions of TGF-beta1, alpha-SMA, and P311 were assessed by quantitative RT-PCR. Protein expressions of TGF-beta1 and alpha-SMA were investigated by Western blotting
Results: Treatment with TMP significantly reduced the proliferation of benign biliary stricture fibroblasts, and significantly attenuated both the mRNA and protein expressions of TGF-beta1, alpha-SMA, and P311 [p <0.05] in a dose-dependent manner
Conclusion: TMP significantly reduced the proliferation of benign biliary stricture fibroblasts, and significantly down- regulated the mRNA/protein expression of TGF-beta1, alpha-SMA, and P311. Therefore, TMP may be a therapeutic option for the prevention of benign biliary stricture