The changes of systemic immune responses during the neuroprotection induced by remote ischemic postconditioning against focal cerebral ischemia in mice.

Abstract:

:Objective: Remote limb ischemic postconditioning (RIPostC) protects the brain from damage induced by transient focal ischemia/reperfusion. However, the underlying mechanism remains unclear. Methods: RIPostC induced by 10 min of occlusion and another 10 min releasing of blood flow for three cycles in the hind limbs was performed immediately after the reperfusion in a focal ischemia mice model. Neurological scores, immune cell population in the blood, spleen and lymph node, and inflammatory factors in the blood and brain were analyzed 2 days after the reperfusion. Results: Our results demonstrate that RIPostC reduced cerebral injuries and improved neurological functions 2 days after reperfusion. RIPostC significantly inhibited the reduction in the percentage of CD4 T cells in the spleen and lymph node, CD8 T cells in the blood and lymph node, and natural killer T (NKT) cells in the spleen by flow cytometry analysis. RIPostC attenuated the increase of B cells and NK cells in the spleen and noninflammatory monocytes in the blood. The cytokine assay showed that RIPostC decreased the elevation of IL-10, IL-6, and TNF-α in the blood after ischemia. The quantitative real time reverse transcription polymerase chain reaction (qRT-PCR) results indicated that the mRNA level of IL-4 in the brain increased in the middle cerebral artery occlusion mice after RIPostC treatment. Conclusions: The present study indicates that there were significant changes of inflammatory responses during the neuroprotection induced by RIPostC in stroke mice.

journal_name

Neurol Res

journal_title

Neurological research

authors

Liu C,Yang J,Zhang C,Geng X,Zhao H

doi

10.1080/01616412.2018.1523037

subject

Has Abstract

pub_date

2019-01-01 00:00:00

pages

26-36

issue

1

eissn

0161-6412

issn

1743-1328

journal_volume

41

pub_type

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