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Limb remote ischaemic postconditioning‐induced elevation of fibulin‐5 confers neuroprotection to rats with cerebral ischaemia/reperfusion injury: Activation of the AKT pathway

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Clinical and Experimental Pharmacology and Physiology

Published online on


Limb remote ischaemic postconditioning (RIPostC) is an effective and well‐acknowledged treatment for brain ischaemia injury. The present study aimed to evaluate the role of fibulin‐5 in the neuroprotection of RIPostC against cerebral ischaemia/reperfusion (I/R) injury in rats. The middle cerebral artery occlusion (MCAO) model was established in rats and then RIPostC was carried out by three cycles of 10 minutes occlusion/10 minutes release of the bilateral femoral artery at the beginning of the reperfusion. To downregulate the fibulin‐5 level, fibulin‐5 siRNA was injected into the lateral ventricle 24 hours before MCAO. According to our present study, RIPostC attenuated cerebral I/R injury by decreasing infarct volume, improving neurobehavioral score and suppressing blood brain barrier (BBB) leakage. Moreover, the mRNA and protein levels of fibulin‐5 were upregulated by RIPostC at 24 hours and 72 hours after reperfusion. Downregulation of fibulin‐5 attenuated the neuroprotection of RIPostC. Finally, the result showed that fibulin‐5 was upregulated by RIPostC via activation of the PI3K/AKT pathway. Taken together, these results provide evidence that upregulation of fibulin‐5 is involved in the beneficial effect of RIPostC against cerebral I/R injury.