neotuberostemonine and Pulmonary-Fibrosis

neotuberostemonine has been researched along with Pulmonary-Fibrosis* in 2 studies

Other Studies

2 other study(ies) available for neotuberostemonine and Pulmonary-Fibrosis

ArticleYear
Neotuberostemonine and tuberostemonine ameliorate pulmonary fibrosis through suppressing TGF-β and SDF-1 secreted by macrophages and fibroblasts via the PI3K-dependent AKT and ERK pathways.
    Chinese journal of natural medicines, 2023, Volume: 21, Issue:7

    Topics: Alkaloids; Animals; Fibroblasts; Macrophages; MAP Kinase Signaling System; Mice; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Pulmonary Fibrosis; Transforming Growth Factor beta

2023
Neotuberostemonine attenuates bleomycin-induced pulmonary fibrosis by suppressing the recruitment and activation of macrophages.
    International immunopharmacology, 2016, Volume: 36

    Neotuberostemonine (NTS) is one of the main antitussive alkaloids in the root of Stemona tuberosa Lour. This study aimed to investigate the effects of NTS on bleomycin (BLM)-induced pulmonary fibrosis in mice and the underlying mechanism. After BLM administration, NTS were orally administered to mice at 20 and 40mg/kg per day from days 8 to 21, with nintedanib as a positive control. The effect of NTS on BLM-induced mice was assessed via histopathological examination by HE and Masson's trichrome staining, TGF-β1 level and macrophage recruitment by immunohistochemical staining, expression of profibrotic media and M1/M2 polarization by western blot. RAW 264.7 cells were used to evaluate whether NTS (1, 10, 100μM) directly affected macrophages. The results revealed that NTS treatment significantly ameliorated lung histopathological changes and decreased inflammatory cell counts in the bronchoalveolar lavage fluid. The over-expression of collagen, α-SMA and TGF-β1 was reduced by NTS. Furthermore, NTS markedly lowered the expression of MMP-2 and TIMP-1 while raised the expression of MMP-9. A further analysis showed that NTS was able to decrease the recruitment of macrophages and to inhibit the M2 polarization in mice lung tissues. The experiment in vitro showed that NTS significantly reduced the arginase-1 (marker for M2) expression in a dose-dependent manner but down-regulated the iNOS (marker for M1) expression only at 100μM. In conclusion, our study demonstrated for the first time that NTS has a significant protective effect on BLM-induced pulmonary fibrosis through suppressing the recruitment and M2 polarization of macrophages.

    Topics: Alkaloids; Animals; Anti-Inflammatory Agents; Bleomycin; Cell Movement; Cells, Cultured; Humans; Immunosuppression Therapy; Lactones; Macrophage Activation; Macrophages, Alveolar; Male; Mice; Mice, Inbred C57BL; Pulmonary Fibrosis; Stemonaceae

2016