Remote ischemic preconditioning (RIPreC) and postconditioning (RIPostC) have been demonstrated to attenuate brain injury after ischemic stroke in healthy animals. This study investigated whether RIPreC and RIPostC exerted neuroprotection against cerebral ischemic injury in type 2 diabetic mice. RIPreC (24 h before ischemia) and RIPostC (immediately after reperfusion) were performed in an ischemia/reperfusion induced stroke model with type 2 diabetes. Ischemic outcomes, flow cytometry, multiplex cytokine assay, and western blotting were analyzed after 45 min of ischemia followed by 48 h of reperfusion. Our data indicated that RIPreC and RIPostC attenuated cerebral injuries and neurological deficits. RIPreC significantly reduced CD4 T cell and CD8 T cell infiltration and increased B cell infiltration into the ischemic brain. It also upregulated CD4 and CD8 T cell levels in the peripheral blood. However, RIPostC significantly decreased CD8 T cells infiltration and increased B cell infiltration into the ischemic brain. RIPreC inhibited IL-6 level in both the brain and blood, while RIPostC treatment attenuated IL-6 level upregulation in the peripheral blood. In addition, both RIPreC and RIPostC significantly increased p-ERK expression in the ipsilateral hemisphere in diabetic mice. This study indicated that RIPreC and RIPostC neuroprotection is present in type 2 diabetic mice via the modulation of brain ERK activity and inflammatory responses in both the peripheral blood and ischemic brain. However, the benefit was lower in RIPostC.

中文翻译：

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远程缺血调节通过调节2型糖尿病小鼠的炎症反应和ERK活性来减少脑缺血损伤。

远程缺血预处理（RIPreC）和后处理（RIPostC）已被证明可以减轻健康动物缺血性中风后的脑损伤。这项研究调查了RIPreC和RIPostC是否对2型糖尿病小鼠的脑缺血损伤发挥了神经保护作用。RIPreC（缺血前24小时）和RIPostC（再灌注后立即）在缺血/再灌注诱发的2型糖尿病中风模型中进行。缺血45分钟后再灌注48小时后，分析缺血结局，流式细胞仪，多重细胞因子测定和蛋白质印迹。我们的数据表明RIPreC和RIPostC减轻了脑损伤和神经功能缺损。RIPreC显着减少了CD4 T细胞和CD8 T细胞的浸润，并增加了B细胞向缺血性脑的浸润。它还上调了外周血中的CD4和CD8 T细胞水平。但是，RIPostC显着降低了CD8 T细胞的浸润并增加了B细胞浸入缺血性脑的能力。RIPreC抑制大脑和血液中的IL-6水平，而RIPostC处理则减弱外周血中IL-6的水平上调。另外，在糖尿病小鼠的同侧半球中，RIPreC和RIPostC都显着增加了p-ERK表达。这项研究表明，RIPreC和RIPostC神经保护作用是通过调节外周血和局部缺血性脑的ERK活性和炎症反应来调节2型糖尿病小鼠的。但是，RIPostC的收益较低。RIPostC显着降低了CD8 T细胞的浸润，并增加了B细胞浸入缺血性脑的渗透。RIPreC抑制大脑和血液中的IL-6水平，而RIPostC处理则减弱外周血中IL-6的水平上调。另外，在糖尿病小鼠的同侧半球中，RIPreC和RIPostC都显着增加了p-ERK表达。这项研究表明，RIPreC和RIPostC神经保护作用是通过调节外周血和局部缺血性脑的ERK活性和炎症反应来调节2型糖尿病小鼠的。但是，RIPostC的收益较低。RIPostC显着降低了CD8 T细胞的浸润，并增加了B细胞浸入缺血性脑的渗透。RIPreC抑制大脑和血液中的IL-6水平，而RIPostC处理则减弱外周血中IL-6的水平上调。另外，在糖尿病小鼠的同侧半球中，RIPreC和RIPostC都显着增加了p-ERK表达。这项研究表明，RIPreC和RIPostC神经保护作用是通过调节外周血和局部缺血性脑的ERK活性和炎症反应来调节2型糖尿病小鼠的。但是，RIPostC的收益较低。糖尿病小鼠的RIPreC和RIPostC都显着增加了同侧半球中p-ERK的表达。这项研究表明，RIPreC和RIPostC神经保护作用是通过调节外周血和局部缺血性脑的ERK活性和炎症反应来调节2型糖尿病小鼠的。但是，RIPostC的收益较低。糖尿病小鼠的RIPreC和RIPostC都显着增加了同侧半球中p-ERK的表达。这项研究表明，RIPreC和RIPostC神经保护作用是通过调节外周血和局部缺血性脑的ERK活性和炎症反应来调节2型糖尿病小鼠的。但是，RIPostC的收益较低。