galangin and Pulmonary-Fibrosis

Pulmonary fibrosis (PF) is a disease that is characterized by abnormal epithelial-mesenchymal transition (EMT) and persistent inflammatory injury, with high mortality and poor prognosis, but the current therapies are accompanied by certain adverse side effects. In this study, we investigated the role of galangin (GA), an anti-inflammatory and anti-tumoral phytochemical extracted from galangal, in preventing and curing bleomycin (BLM)-induced pulmonary fibrosis and the underlying mechanism. Histopathological staining confirmed that GA dramatically moderated bleomycin-induced pulmonary fibrosis in mice. Compared with the vehicle treatment, GA treatment inhibited the expression of vimentin and increased the expression of E-cadherin. The expression of α-Smooth muscle actin (α-SMA), which is a myofibroblast marker, was also suppressed. In addition, GA diminished the increase in the numbers of CD4

Topics: A549 Cells; Animals; Anti-Inflammatory Agents; Antineoplastic Agents, Phytogenic; Bleomycin; Cell Survival; Dose-Response Relationship, Drug; Epithelial-Mesenchymal Transition; Flavonoids; Humans; Male; Mice; Mice, Inbred C57BL; Molecular Structure; Phytochemicals; Pulmonary Fibrosis; Structure-Activity Relationship; Tumor Cells, Cultured