title: Astaxanthin ameliorates lung fibrosis in vivo and in vitro by preventing transdifferentiation, inhibiting proliferation, and promoting apoptosis of activated cells.
abstract: Astaxanthin, a member of the carotenoid family, is the only known ketocarotenoid transported into the brain by transcytosis through the blood-brain barrier. However, whether astaxanthin has antifibrotic functions is unknown. In this study, we investigated the effects of astaxanthin on transforming growth factor β1-mediated and bleomycin-induced pulmonary fibrosis in vitro and in vivo. The results showed that astaxanthin significantly improved the structure of the alveoli and alleviated collagen deposition in vivo. Compared with the control group, the astaxanthin-treated groups exhibited downregulated protein expressions of α-smooth muscle actin, vimentin, hydroxyproline, and B cell lymphoma/leukemia-2 as well as upregulated protein expressions of E-cadherin and p53 in vitro and in vivo. Astaxanthin also inhibited the proliferation of activated A549 and MRC-5 cells at median inhibitory concentrations of 40 and 30 μM, respectively. In conclusion, astaxanthin could relieve the symptoms and halt the progression of pulmonary fibrosis, partly by preventing transdifferentiation, inhibiting proliferation, and promoting apoptosis of activated cells.
authors.affiliation: Medicine Research Center, Binzhou Medical University, Yantai 264003, China.
authors.forename: Meirong
authors.initials: M
authors.lastname: Wang
authors.forename: Jinjin
authors.initials: J
authors.lastname: Zhang
authors.forename: Xiaodong
authors.initials: X
authors.lastname: Song
authors.forename: Wenbo
authors.initials: W
authors.lastname: Liu
authors.forename: Lixia
authors.initials: L
authors.lastname: Zhang
authors.forename: Xiuwen
authors.initials: X
authors.lastname: Wang
authors.forename: Changjun
authors.initials: C
authors.lastname: Lv
mesh_terms: D000199:Actins / Q000235:genetics / Q000378:metabolism; D015703:Antigens, CD; D017209:Apoptosis / Q000187:drug effects*; D001761:Bleomycin / Q000009:adverse effects / Q000378:metabolism; D001812:Blood-Brain Barrier / Q000187:drug effects / Q000378:metabolism; D015820:Cadherins / Q000235:genetics / Q000378:metabolism; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects*; D054338:Cell Transdifferentiation / Q000187:drug effects*; D003094:Collagen / Q000378:metabolism; D015536:Down-Regulation; D006801:Humans; D006909:Hydroxyproline / Q000235:genetics / Q000378:metabolism; D008168:Lung / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D046529:Microscopy, Electron, Transmission; D011650:Pulmonary Alveoli / Q000187:drug effects / Q000378:metabolism; D011658:Pulmonary Fibrosis / Q000517:prevention & control*; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation; D014746:Vimentin / Q000235:genetics / Q000378:metabolism; D024341:Xanthophylls / Q000494:pharmacology
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; D015703:Antigens, CD; C513384:CDH1 protein, human; D015820:Cadherins; C495901:TP53 protein, human; D053773:Transforming Growth Factor beta1; D016159:Tumor Suppressor Protein p53; D014746:Vimentin; D024341:Xanthophylls; D001761:Bleomycin; C005948:astaxanthine; D003094:Collagen; D006909:Hydroxyproline