ABSTRACT
Objective: To investigate the effects of thrombopoietin (TPO) on proliferation and collagen synthesis in pulmonary fibro-blasts induced by TGFβ1. Methods: Cultured human embryonic lung fibroblasts (HFLs) were treated with recombinant human TGF-β1 to induce myofibroblast differentiation. Different concentrations of recombinant human TPO were applied individually or in combina-tion. Cell proliferation rate was determined using the CCK8 assay. Q-PCR and immunofluorescence assay were employed to examine the mRNA and protein expression of α-smooth muscle actin (αSMA) and type I collagen (COL1)A2. Results: TGFβ1 treatment induced HFL transdifferentiation to myofibroblasts was determined by the expression of αSMA, a myofibroblast-specific marker. Cell prolifera-tion increased during the induction. COL1 gene and protein expression were upregulated by TGFβ1 induction (P<0.05). The TGFβ1-in-duced mRNA and protein expression of αSMA and COL1A2 was decreased by TPO treatment (P<0.05), as determined by reverse tran-scription quantitative polymerase chain reaction and immunofluorescence analysis, respectively. The inhibitory rate showed a dose de-pendent effect within a certain TPO concentration range. The CCK8 assay demonstrated that TPO downregulated the TGFβ1-induced proliferation (P<0.05). Furthermore, the expression of heme oxygenase-1 (HO-1) was downregulated in TGFβ1-induced lung fibro-blasts, and these effects were attenuated by TPO administration (P<0.05). Conclusions: TPO can inhibit the TGFβ1-induced prolifera-tion and differentiation of human lung fibroblasts. These effects may be mediated in part by HO-1-related signaling pathways.
ABSTRACT
AIM: To study the anti-atherogenesis action of sodium ferulate and its mechanisms. METHODS: Atherosclerotic rabbit models were duplicated by feeding high lipid forage and ECV304 were cultured with the hyperlipidemic serum. The atherosclerotic plaque area was measured. Scanning electron microscope, spectrophotometer and immunocytochemical methods were used to detected the microstructures of endothelial cell, the content of NO in suspension and the expressions of TGFβ1, bFGF on the cell surfaces. RESULTS: Sodium ferulate could decrease the plaque area, lessen the damnification of endothelial cell induced by HLS, enhance the expression of TGFβ1 and the release of NO from ECs, and reduce the expressions of bFGF in ECs, significantly. CONCLUSION: Sodium ferulate can decrease the atherosclerotic plaque area induced by hypercholesterol, which may be relate to the expression change of cytokines.