Remote ischemic conditioning reduced cerebral ischemic injury by modulating inflammatory responses and ERK activity in type 2 diabetic mice.

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.

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Declaration of competing interest The authors declare that they have no conflict of interest.