Tanshinone IIA alleviates bleomycin-induced pulmonary fibrosis by inhibiting Zbtb16.

Pulmonary fibrosis is a complex disease that can occur in a variety of clinical settings. The Zinc Finger and BTB Domain Containing 16 (Zbtb16) is a transcription factor and has not been studied in pulmonary fibrosis. Lung tissues from rats which were treated with bleomycin and Tanshinone IIA (Tan IIA) were collected for mRNA sequencing. Zbtb16, a differentially expressed gene, was screened. Using adeno-associated virus to knock down Zbtb16 in rats, it was found that the lung index and the content of hydroxyproline in lung tissue were decreased. HE and Masson staining revealed that pathological symptoms of lung histopathology were relieved after Zbtb16 knockdown. Protein expressions of α-SMA, Collagen I and Fibronectin were significantly decreased after Zbtb16 knockdown in vivo and in vitro. Meanwhile, the protein content of TGF-ß1 and the phosphorylation of Smad2/3 were inhibited by Zbtb16 knockdown. Conversely, under the treatment of Tan IIA and TGF-ß1, overexpression of Zbtb16 improved cell viability, increased the expression of fibrosis-related proteins, and promoted the phosphorylation of Smad 2/3. All above demonstrates that Zbtb16 inhibition ameliorates pulmonary fibrosis and suppresses the TGF-ß/Smad pathway. Furthermore, Zbtb16 mediates the inhibitory process of Tan IIA on pulmonary fibrosis. This study provides a novel candidate therapeutic target for pulmonary fibrosis.

Soufeng Yuchuan decoction mitigates the ovalbumin-induced lung damage in a rat model of asthma.

Airway remodeling is a key feature of asthma. Extracellular matrix synthesis and vascular remodeling respectively regulated by transforming growth factor (TGF-ß1) and vascular endothelial growth factor (VEGF), are important for the airway remodeling. This study aimed to investigate the effect of Soufeng Yuchuan (SFYC) decoction, a Traditional Chinese Medicine, on airway remodeling and expression of VEGF and TGF-ß1 in asthma model rats. A rat model of asthma was induced by ovalbumin (OVA) treatment. The results showed that SFYC decoction improved general conditions and reduced the damage in lung tissues in asthma model rats. Furthermore, SFYC decoction significantly reduced the OVA-induced levels of VEGF and TGF-ß1 in sera and in bronchoalveolar lavage fluid. Moreover, SFYC decoction decreased the OVA-induced VEGF mRNA and protein levels in lung tissues in asthma model rats. Interestingly, SFYC with high dose was more potent in reducing TGF-ß1 level in rat sera and BALF than dexamethasone (positive control). In summary, SFYC decoction effectively mitigates lung damage in OVA-induced asthma model rats, which was associated with inhibition of VEGF and TGF-ß1.