Journal
CNS NEUROSCIENCE & THERAPEUTICS
Volume 18, Issue 11, Pages 903-908Publisher
WILEY-BLACKWELL
DOI: 10.1111/cns.12000
Keywords
Apoptosis; E-selectin; Inflammation; Ischemic stroke
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Funding
- National Natural Science Foundation of China [30730106]
- National Basic Research Program of China (973 Program) [2009CB521901]
- National Scientific and Technological Major Special Project for Significant Creation of New Drugs [2008ZXJ 09014-0095]
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Aims: To determine whether E-selectin deficiency can attenuate brain ischemia in a mouse model of focal cerebral ischemia. Methods: E-selectin was determined in spontaneously hypertensive rats (SHRs) and stroke-prone spontaneously hypertensive rats (SHR-SPs). E-selectin knockout (Es-/-) mice and wild-type control (WT) mice underwent permanent distal middle cerebral artery occlusion (MCAO). Behavioral analyses were performed followed by the measurement of infarct areas. Myeloperoxidase (MPO) protein was determined by Western blot. IL-6, IL-1 beta, and TNF-alpha were detected by ELISA. In situ detection of apoptotic cells was performed by TUNEL staining. Results: The brain and serum E-selectin levels were higher in SHR-SPs than in SHRs (P < 0.05) after salt intake. E-selectin deficiency improved neurological function and reduced infarct area in cerebral ischemic mice. MPO and IL-1 beta were lower in Es-/- mice than in WT mice. In addition, the number of apoptotic cells in Es-/- mice was significantly less than in WT mice after MCAO. Conclusions: E-selectin deficiency presents protective effect on cerebral ischemia. This protective effect is likely achieved by the inhibition of inflammation and apoptosis.
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