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首页> 外文期刊>CNS neuroscience & therapeutics. >Exosomes containing miR-451a is involved in the protective effect of cerebral ischemic preconditioning against cerebral ischemia and reperfusion injury
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Exosomes containing miR-451a is involved in the protective effect of cerebral ischemic preconditioning against cerebral ischemia and reperfusion injury

机译：含有miR-451a的外泌体参与脑缺血预处理对脑缺血和再灌注损伤的保护作用

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Aim To study the role of exosomes in the protective effect of cerebral ischemic preconditioning (cerebral-IPC) against cerebral I/R injury. Method Mouse models of cerebral-IPC and MCAO/R were established as described previously, and their behavioral, pathological, and proteomic changes were analyzed. Neuro-2a subjected to OGD/R were treated with exosomes isolated from the plasma of sham-operated and cerebral-IPC mice. The differentially expressed miRNAs between exosomes derived from sham-operated (S-exosomes) and preconditioned (IPC-exosomes) mice were identified through miRNA array, and their targets were identified through database search. The control and OGD/R cells were treated with the IPC-exosomes, miRNA mimic or target protein inhibitor, and their viability, oxidative, stress and apoptosis rates were measured. The activated pathways were identified by analyzing the levels of relevant proteins. Results Cerebral-IPC mitigated the cerebral injury following ischemia and reperfusion, and increased the number of plasma exosomes. IPC-exosomes increased the survival of Neuro-2a cells after OGD/R. The miR-451a targeting Rac1 was upregulated in the IPC-exosomes relative to S-exosomes. The miR-451a mimic and the Rac1 inhibitor NSC23766 reversed OGD/R-mediated activation of Rac1 and its downstream pathways. Conclusion Cerebral-IPC ameliorated cerebral I/R injury by inducing the release of exosomes containing miR-451a.
机译：目的研究外来体在脑缺血预处理（脑-IPC）对脑I / R损伤的影响中的作用。如前所述建立了脑-IPC和MCAO / R的方法小鼠模型，并分析了它们的行为，病理和蛋白质组学变化。用从假手术和脑-IPC小鼠的血浆中分离的外来分离的外泌体对经受OGD / R进行的神经2A。通过MiRNA阵列鉴定衍生自假手术（S-外肌肉）和预处理（IPC-Exosomes）小鼠的外索体之间的差异表达的miRNA，通过数据库搜索鉴定它们的靶标。用IPC-Exosomes，miRNA模拟物或靶蛋白抑制剂处理对照和OGD / R细胞，并测量它们的活力，氧化，应力和凋亡率。通过分析相关蛋白质的水平来鉴定活化的途径。结果脑IPC减轻缺血再灌注后的脑损伤，并增加了血浆外泌体的数量。 IPC-Exosomes在OGD / R后增加神经2A细胞的存活。靶向RAC1的MIR-451A相对于S-EXOSOMES在IPC-EXOSOMES中上调。 miR-451a模拟和Rac1抑制剂NSC23766反转OGD / R介导的RAC1和下游途径的激活。结论脑IPC改善脑I / R损伤，诱导含有miR-451a的外泌体释放。

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