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Bone marrow mesenchymal stem cell-derived exosomes attenuate cerebral ischemia-reperfusion injury-induced neuroinflammation and pyroptosis by modulating microglia M1/M2 phenotypes.

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机构： [1]Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China [2]School of rehabilitation medicine, southern medical university, Guangzhou, China [3]Department of Rehabilitation, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, China [4]Department of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou, Guangdong Province, China [5]Department of Neurorehabilitation, Xiangya Boai Rehabilitation Hospital, Changsha, China [6]Department of Rehabilitation Medicine, Hunan Provincial People's Hospital, Hunan Normal University, Changsha, China [7]Department of Traditional Chinese Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China

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关键词： BMSC-Exosomes Cerebral Ischemia-Reperfusion Injury Neuroinflammation Pyroptosis Microglial Polarization

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Pyroptosis mediated by NLRP3 inflammasome plays a critical role in the pathogenesis of cerebral ischemia-reperfusion (I/R) injury. Mounting evidences have verified the efficacy of exosomes by relieving the inflammatory response during cerebral I/R injury, but the specific mechanism has not been well elucidated. This study aimed to clarify whether the neuroprotective effects of bone marrow mesenchymal stem cell-derived exosomes (BMSC-Exos) are associated with the attenuation of NLPR3-mediated neuron pyroptosis by modulating microglial polarization. Rats were initially subjected to middle cerebral artery occlusion (MCAO) followed by reperfusion. Then, BMSC-Exos were administered intravenously 2 h after MCAO. The neuroprotective effects were measured using a modified neurological severity score, triphenyltetrazolium chloride (TTC) staining, brain water content, Morris water maze, and CatWalk system. Western blotting and immunofluorescence staining were applied to detect NLRP3 inflammasome and pyroptosis. Microglial polarization was determined by real-time polymerase chain reaction (RT-PCR) and immunofluorescence staining. To mimic cerebral I/R injury in vitro, BV2 and PC12 cells were exposed to oxygen-glucose deprivation/reoxygenation. After treatment with PBS, BMSC-Exos, IL-4, or LPS, BV2 cells were co-cultured with PC12 cells in a Transwell system. BMSC-Exos reduced the brain infarct area and brain water content at 24 h dose dependently and improved the neurological function up to 5 weeks after stroke. In vivo, NLRP3 inflammasome- and pyroptosis-related proteins were mainly expressed on neurons and downregulated by BMSC-Exos. Furthermore, cerebral I/R injury-induced M1-polarized microglia could be shifted toward M2 phenotype by BMSC-Exos. In vitro, BMSC-Exos alleviated the neuron pyroptosis partially by modulating microglial polarization. BMSC-Exos could ameliorate cerebral I/R injury via suppression of NLRP3 inflammasome-mediated inflammation and pyroptosis by modulating microglial polarization. Copyright © 2021. Published by Elsevier Inc.

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出版当年[2020]版：

大类 | 2 区医学

小类 | 2 区神经科学

最新[2025]版：

大类 | 2 区医学

小类 | 2 区神经科学

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出版当年[2019]版：

Q1 NEUROSCIENCES

最新[2023]版：

Q1 NEUROSCIENCES

影响因子： 4.6 最新[2023版] 4.8 最新五年平均 4.691 出版当年[2019版] 4.767 出版当年五年平均 4.562 出版前一年[2018版] 5.33 出版后一年[2020版]

第一作者：

第一作者机构： [1]Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China [2]School of rehabilitation medicine, southern medical university, Guangzhou, China

通讯作者：

通讯机构： [1]Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China [2]School of rehabilitation medicine, southern medical university, Guangzhou, China

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Bone marrow mesenchymal stem cell-derived exosomes attenuate cerebral ischemia-reperfusion injury-induced neuroinflammation and pyroptosis by modulating microglia M1/M2 phenotypes. $(function () { $("[data-toggle='tooltip']").tooltip(); });

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Bone marrow mesenchymal stem cell-derived exosomes attenuate cerebral ischemia-reperfusion injury-induced neuroinflammation and pyroptosis by modulating microglia M1/M2 phenotypes.