In the pathological process of the lungs, excessive deposition of extracellular matrix (ECM) and epithelial mesenchymal transition (EMT) are typical hallmark features of pulmonary fibrosis. Excessive deposition of ECM can disrupt the normal structure of the lungs. EMT causes epithelial cells to lose their original characteristics and transform into more invasive stromal cells. The joint promotion of the two can lead to pulmonary fibrosis in the body, which is a disease that progresses over time and can cause significant decline in respiratory function. Salvia miltiorrhiza contains a bioactive compound called cryptotanshinone (CTS), which has been shown to have antifibrotic effects. The aim of this research is to investigate how CTS helps to mitigate pulmonary fibrosis. Used TGF-β to treat the pulmonary fibrosis state exhibited by A549 cells. Western blotting, immunofluorescence, ELISA, flow cytometry, and CCK-8 assays were employed to evaluate the effects of CTS on EMT markers, fibrosis-related proteins, cytokines, apoptosis, and proliferation. Immunofluorescence could visually present the distribution of proteins within cells. Co-treatment with the AKT activator SC79 was used to evaluate the PI3K/AKT pathway's involvement. CTS inhibited TGF-β-induced EMT. It could downregulate the levels of fibrosis-related proteins and pro-inflammatory cytokines, promote cell apoptosis, inhibit cell proliferation, and exert multiple regulatory effects in fibrotic A549 cells. CTS promoted apoptosis and suppressed cell proliferation. Mechanistic studies revealed that CTS inhibited PI3K and AKT phosphorylation, with these effects reversed by SC79, confirming the involvement of the PI3K/AKT pathway. CTS mitigates pulmonary fibrosis by inhibiting PI3K/AKT-mediated EMT, supporting its potential as a therapeutic agent for pulmonary fibrosis.
Liu et al. (Sun,) studied this question.