Basic & Clinical Medicine ›› 2023, Vol. 43 ›› Issue (5): 771-776.doi: 10.16352/j.issn.1001-6325.2023.05.0771

• Original Articles • Previous Articles     Next Articles

Protective effect of BM-MSCs-derived exosome-mediated ferroptosis against anoxia-reoxygenation injury in rat cardiomyoblastl cell line H9c2

YAN Lin, LU Juexiu, LUO Ying, LIU Xianxia*   

  1. Department of Cardiovascular Medicine, the Second Affiliated Hospital of Hainan Medical University,Haikou 570100, China
  • Received:2022-11-13 Revised:2023-03-22 Online:2023-05-05 Published:2023-04-26
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Abstract: Objective To investigate the protective effect and molecular mechanism of bone marrow mesenchymal stem cells(BM-MSCs)-derived exosomes against anoxia-reoxygenation (A/R) injury in rat cardiomyoblast cell line H9c2. Methods The A/R injury model of H9c2 cells was constructed. Electron microscopy and Western blot were used to identify BM-MSCs-derived exosomes(BM-MSCs-exos); PHK26 red fluorescence-labeled exosomes were used to observe the endocytosis of H9c2 cells; CCK-8 assay was used to detect cell viability; EdU cell proliferation assay was used to detect cell proliferation ability; Ferroptosis-related detection kits were used to determine Fe2+, MDA, GSH content; Flow cytometry was used to detect reactive oxygen species free radical ROS level. Results BM-MSCs-exos were successfully identified, and the endocytosis of BM-MSCs-exos by H9c2 cells was found. Compared with A/R group, cell viability and proliferation in A/R+ MSCs-exo group were significantly improved (P<0.05).Ferroptosis marker protein GPX4, SLC7A11 increased; Transferrin receptor TFR1 expression decreased(P<0.05); And Fe2+ ions, MDA, ROS all decreased while GSH increased(P<0.05). After treatment with the ferroptosis inducer Erastin, the protective effect of BM-MSCs-exo against A/R injury in H9c2 cells was significantly reduced (P<0.05). Conclusions BM-MSCs-exos can alleviate A/R-induced cardiomyocyte injury, and is potentially mediated by inhibiting cardiomyocyte ferroptosis.

Key words: exosomes, ferroptosis, cardiomyoblast cell line H9c2, anoxia-reoxygenation

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