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Mesenchymal Stem Cell-Conditioned Medium Protects Hippocampal Neurons From Radiation Damage by Suppressing Oxidative Stress and Apoptosis.
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- Author(s): Huang, Yue1 (AUTHOR); Mei, Xiaolong2 (AUTHOR); Jiang, Weishi1 (AUTHOR); Zhao, Hui3 (AUTHOR); Yan, Zhenyu4 (AUTHOR); Zhang, Haixia4 (AUTHOR); Liu, Ying1 (AUTHOR); Hu, Xia1 (AUTHOR); Zhang, Jingyi1 (AUTHOR); Peng, Wenshuo1 (AUTHOR); Zhang, Jing5,6,7,8 (AUTHOR) ; Qi, Qingling9 (AUTHOR) ; Chen, Naiyao4 (AUTHOR)
- Source:
Dose-Response. Jan-Mar2021, Vol. 19 Issue 1, p1-10. 10p.
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- Additional Information
- Abstract:
Objective: To investigate the effects of mesenchymal stem cell-conditioned medium (MSC-CM) on radiation-induced oxidative stress, survival and apoptosis in hippocampal neurons. Methods: The following groups were defined: Control, radiation treatment (RT), RT+MSC-CM, MSC-CM, RT + N-Acetylcysteine (RT+NAC), and RT + MSC-CM + PI3 K inhibitor (LY294002). A cell Counting Kit-8 (CCK-8) was used to measure cell proliferation. Apoptosis was examined by AnnexinV/PI flow cytometric analyses. Intracellular reactive oxygen species (ROS) were detected by DCFH-DA. Intracellular glutathione (GSH), malondialdehyde (MDA) content, and superoxide dismutase (SOD) activity were detected by colorimetric assays. Protein levels of γ-H2AX, PI3K-AKT, P53, cleaved caspase-3, Bax, and BCl-2 were analyzed by Western blotting. Results: The proliferation of HT22 cells was significantly inhibited in the RT group, but was significantly preserved in the RT + MSC-CM group (P < 0.01). Apoptosis was significantly higher in the RT group than in the RT+ MSC-CM group (P < 0.01). MSC-CM decreased intracellular ROS and MDA content after irradiation (P < 0.01). GSH level and SOD activity were higher in the RT + MSC-CM group than in the RT group, as was MMP (P < 0.01). MSC-CM decreased expression of γ-H2AX, P53, Bax, and cleaved-caspase-3, but increased Bcl-2 expression (P < 0.01). Conclusion: MSC-CM attenuated radiation-induced hippocampal neuron cell line damage by alleviating oxidative stress and suppressing apoptosis. [ABSTRACT FROM AUTHOR]
- Abstract:
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