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⁺CD69⁺ and CD8⁺CD69⁺ T cells and dendritic cells induced by bleomycin, and reduced the residence of inflammatory cells in the lung tissues. Notably, GA inhibited the TGF-β1-induced EMT and fibroblast differentiation in vitro, which further confirmed the potential protective effect of GA on pulmonary fibrosis. Taken together, our results suggest that GA exerts a beneficial effect on bleomycin-induced pulmonary fibrosis by attenuating EMT and inflammatory damage and may have prevent potential of pulmonary fibrosis.

肺纤维化（PF）是一种以异常的上皮-间质转化（EMT）和持续性炎性损伤为特征的疾病，具有高死亡率和预后不良，但目前的疗法伴随着某些不良副作用。在这项研究中，我们调查了从高良姜中提取的抗炎和抗肿瘤植物化学成分高良姜素（GA）在预防和治疗博来霉素（BLM）诱导的肺纤维化中的作用及其潜在机制。组织病理学染色证实GA显着减轻了博来霉素诱导的小鼠肺纤维化。与媒介物处理相比，GA处理抑制波形蛋白的表达并增加E-钙粘蛋白的表达。肌成纤维细胞标志物α-平滑肌肌动蛋白（α-SMA）的表达也被抑制。此外，博来霉素诱导的⁺ CD69 ⁺和CD8 ⁺ CD69 ⁺ T细胞和树突状细胞减少了炎症细胞在肺组织中的滞留。值得注意的是，GA在体外抑制了TGF-β1诱导的EMT和成纤维细胞分化，这进一步证实了GA对肺纤维化的潜在保护作用。两者合计，我们的结果表明，GA通过减弱EMT和炎症损伤对博来霉素诱导的肺纤维化发挥有益作用，并可能预防肺纤维化的可能性。