Rehmannia Radix Extract Relieves Bleomycin-Induced Pulmonary Fibrosis in Mice via Transforming Growth Factor β1 (TGF-β1)

Background: Infants and young children with acute respiratory distress syndrome (ARDS) have acute progressive hypoxic respiratory failure caused by a variety of extrapulmonary pathogenic factors and cardiogenic factors. Diffuse alveolar injury and pulmonary fibrosis both are pathological features of ARDS. This study investigated the effect of Rehmannia Radix extract (RRE) on pulmonary fibrosis of infants with ARDS. Material/Methods: The human lung fibroblasts cell line HFL1 was treated with various concentrations of Rehmannia Radix extract in different groups for different times. Flow cytometry and TUNEL assay were performed to detect cell apoptosis, and CCK8 assay was utilized to analyze cell proliferation. TGF-beta 1 expression was detected by real-time quantitative PCR, and protein-level expressions of Caspase3, TGF-beta 1, Bcl-2, and Smad3 were measured by western blot and immunohistochemical staining in cells or tissues. TGF-beta 1 was overexpressed by recombinant human TGF-beta 1 (2 ng/mL) and the treated cells and culture supernatant were harvested for analysis in each step. Bleomycin was used to induce a mouse model of pulmonary fibrosis and was confirmed by HE pathological sections. Results: Flow cytometry and TUNEL results showed that RRE promoted the apoptosis of HFL1 cells in a concentration dependent manner, and it inhibited the proliferation of HFL1 cells. Upregulation of TGF-beta 1 reversed the effects of RRE in HFL1 cells. RRE alleviated pulmonary fibrosis in mice through downregulating Bcl-2, TGF-beta 1, and Smad3 expression. Conclusions: RRE promoted apoptosis and inhibited proliferation of HFL1, and then arrested the progression of pulmonary fibrosis. RRE had a significant inhibitory effect on TGF-beta 1 and Smad3. These results suggest that RRE directly prevents the development of pulmonary fibrosis by affecting the expression of TGF-beta 1 and Smad3.