Protective Effect of Anthocyanin on Paraquat-Induced Apoptosis and Epithelial-Mesenchymal Transition in Alveolar Type II Cells

BACKGROUND: Paraquat (PQ) can over-accumulate in alveolar epithelial cells. Anthocyanin (An) can exert anti-oxidative properties. The role of An in PQ-induced toxicity is unclear, so we aimed to explore whether An could inhibit epithelial mesenchymal transition (EMT) induced by PQ in alveolar cells. MATERIAL/METHODS: Alveolar epithelial cells were treated with PQ and An with concentration gradient for 12, 24, and 48 h. The cell viability, ROS level, and apoptosis rate were determined using the Cell Counting Kit-8 (CCK-8) and flow cytometry, respectively. The lactate dehydrogenase (LDH) leakage, methane dicarboxylic aldehyde (MDA) level, glutathione peroxidase (GPx), and superoxide dismutase (SOD) activities were determined by spectrophotometric method. The mRNA and protein expressions were detected using quantitative real-time PCR (qPCR) and Western blot, respectively. RESULTS: An reduced the PQ-induced apoptosis in a dose-dependent manner. Moreover, An reduced the ratio of Bax/Bcl-2 to ROS level. We found that An suppressed the activity of LDH and MDA and improved SOD and GPX levels. Additionally, the level of PQ-induced E-cadherin was decreased by An while the expressions of vimentin, α-smooth muscle actin (α-SMA), and collagens type I (col-I) were increased. Furthermore, An inhibited the levels of transforming growth factor β1 (TGF-β1) and activin receptor-like kinase 5 (ALK5) and reduced the phosphorylation of smad2. CONCLUSIONS: Our study shows newly discovered effects of anthocyanidins on EMT and supports their chemopreventive effects in paraquat-induced apoptosis in alveolar type II cells.