In addition, although both containing Salvia miltiorrhiza, DLP but not DHP mitigates BLM-induced lung fibrosis by inhibiting the TGF-β signaling-activated myofibroblast differentiation and α-SMA expression in a mouse model.
As a result, from the comparison of multiple factors (α-SMA, collagen type I/III, HYP, MDA, SOD) between pirfenidone group and CN group, it revealed the beneficial effects of CN against BLM-induced and TGF-β<sub>1</sub>-induced pulmonary fibrosis.
MiR-34b-5p knockdown in vivo attenuated the bleomycin-induced pulmonary fibrosis in wild-type mice, displayed by a reduced expression of Col1A1, fibronectin (Fn), and α-SMA.
Moreover, we found that CTS is superior to prednisone in attenuating collagen deposition and pulmonary fibrosis, in parallel with a marked drop of HYP (a collagen indicator) and <i>α</i>-SMA (a myofibroblast marker).
Our results showed that the elevated leptin level in serum correlated with the severity of lung fibrosis and leptin significantly promoted the EMT in A549 cells as evidenced by promoting collagen I and α-SMA production.
In addition, the expression of EMT markers (N-cadherin, vimentin, α-SMA and CTGF) were significantly increased indicating their role in silica induced pulmonary fibrosis.
The DNA-protein pulldown analysis proved that HMGB34367 acted as a novel transcriptional factor for the <i>α</i>-SMA promoter and participated in the eventual development of pulmonary fibrosis.
Furthermore, overexpression of VTN significantly increased the expression level of α-SMA, as well as the degree of lung fibrosis in mice at 8 and 12 weeks post-irradiation.
In a mouse model of lung fibrosis, oral administration of NTS (30 mg·kg<sup>-1</sup>·d<sup>-1</sup>, for 1 or 2 weeks) effectively attenuated bleomycin-induced pulmonary fibrosis by inhibiting the levels of HIF-1α and its downstream profibrotic factors (TGF-β, FGF2 and α-SMA).
Moreover, high levels of extracellular adenosine increase the expression, the production and the activation of pro-fibrotic proteins (such as TGF-β, α-SMA, etc.) followed by the establishment of lung fibrosis.
Taken advantage of this model, we measured body weight loss, lung fibrogenic genes (<i>Acta2</i>, <i>Col1a1</i>, <i>Fsp1</i>, and <i>Fstl1</i>), histology, Masson's trichrome staining, hydroxyproline levels, and expression of α-SMA at protein levels in the BLM-challenged lung for evaluating severity of lung fibrosis.
We found that vimentin and α-SMA-positive cells of the MTX-induced pulmonary fibrosis were increased; on the other hand, E-cadherin was decreased, indicating that epithelial cells act as the main source of mesenchymal expansion.