Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 39, Issue 7, Pages 1215-1231Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X18808174
Keywords
Blood-brain barrier; ischemic stroke; inflammation; microglia; white matter injury
Categories
Funding
- National Key R&D Program from China Ministry of Science Technology [2017YFC1308401, 2016YFC1301502]
- Beijing Municipal Administration [ZYLX201706, SML20150802]
- China Ministry of Higher Education
- China Scholarship Council [201606100182]
- National Natural Science Foundation of China [81871022]
- Competitive Medical Research Fund from the University of Pittsburgh Medical Center (UPMC) Health System
- Pittsburgh Institute of Brain Disorders & Recovery and Department of Neurology at the University of Pittsburgh
- China Ministry of Science Technology
- Beijing Municipal Administration
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Ischemic injury can be alleviated by the judicious use of hypothermia. However, the optimal regimens and the temporal kinetics of post-stroke neurovascular responses to hypothermic intervention have not been systematically studied. These gaps slow the clinical translation of hypothermia as an anti-stroke therapy. Here, we characterized the effects of transient selective brain hypothermia (TSBH) from the hyperacute to chronic stages of focal ischemia/reperfusion brain injury induced by transient middle cerebral artery occlusion in mice. A simple cooling device was used to induce TSBH during cerebral ischemia. This treatment reduced mortality from 31.8% to 0% and improved neurological outcomes for at least 35 days post-injury. TSBH mitigated blood-brain barrier leakage during the hyperacute and acute injury stages (1-23 h post-reperfusion). This early protection of the blood-brain barrier was associated with anti-inflammatory phenotypic polarization of microglia/macrophages, reduced production of pro-inflammatory cytokines, and less brain infiltration of neutrophils and macrophages during the subacute injury stage (three days post-reperfusion). TSBH elicited enduring protective effects on both grey and white matter for at least 35 days post-injury and preserved the long-term electrophysiological function of fiber tracts. In conclusion, TSBH ameliorates ischemia/reperfusion injury in the neurovascular unit from hyperacute to chronic injury stages after experimental stroke.
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