Retracted: Rehmannia Radix Extract Relieves Bleomycin-Induced Pulmonary Fibrosis in Mice via Transforming Growth Factor ß1 (TGF-ß1).

The authors have requested retraction due to the identification of errors in the data. Reference: Xiaoming Hu, Dongzhe Zhu. Rehmannia Radix Extract Relieves Bleomycin-Induced Pulmonary Fibrosis in Mice via Transforming Growth Factor ß1 (TGF-ß1). Med Sci Monit, 2020; 26: e927240. DOI: 10.12659/MSM.927240.

Current epidemiology and factors contributing to postnatal growth restriction in very preterm infants in China.

BACKGROUND: Postnatal growth restriction (PGR) is common in very preterm infants (VPIs) and is associated with adverse short and long-term developmental outcomes. Postnatal growth status for VPIs in middle- or low-income countries remains unclear. AIMS: To evaluate PGR in VPIs and identify maternal and neonatal factors, clinical practice, and major neonatal morbidities associated with PGR in China. STUDY DESIGN: Prospective cohort study. SUBJECTS: We included 6085 infants born at <32 weeks gestation who were admitted at 57 hospitals in the Chinese Neonatal Network in 2019. OUTCOME MEASURES: Birth and discharge weights were converted to age-specific Z-scores. PGR was defined as a decrease in weight z-score from birth to discharge >2. RESULTS: The overall incidence of PGR was 19.9 %. The mean (standard deviation [SD]) weight Z-score was 0.12 (0.78) at birth and decreased to -1.36 (0.98) at discharge. About 4.0 % of VPIs were small for gestational age (SGA) at birth and 25.5 % of SGA infants had PGR. The incidence of PGR increased with decreasing gestational age except in the SGA subgroup. Each 1-unit increase in birthweight Z-score was associated with a 1.49-fold increased risk for PGR. Late initiation of enteral feeds and late achievement of full enteral feeds were positively associated with PGR. The common morbidities that influenced PGR were necrotizing enterocolitis ≥ stage II, patent ductus arteriosus requiring medical or surgical treatment, sepsis, bronchopulmonary dysplasia, and respiratory distress syndrome requiring surfactants. CONCLUSION: Nearly one fifth of VPIs were PGR, and one fourth of SGA had PGR, which warranted further study to investigate underlying causes by which to improve postnatal growth in very preterm infants in future.

Rehmannia Radix Extract Relieves Bleomycin-Induced Pulmonary Fibrosis in Mice via Transforming Growth Factor ß1 (TGF-ß1).

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 AND 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-ß1 expression was detected by real-time quantitative PCR, and protein-level expressions of Caspase3, TGF-ß1, Bcl-2, and Smad3 were measured by western blot and immunohistochemical staining in cells or tissues. TGF-ß1 was overexpressed by recombinant human TGF-ß1 (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-ß1 reversed the effects of RRE in HFL1 cells. RRE alleviated pulmonary fibrosis in mice through downregulating Bcl-2, TGF-ß1, 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-ß1 and Smad3. These results suggest that RRE directly prevents the development of pulmonary fibrosis by affecting the expression of TGF-ß1 and Smad3.