Open AccessE‐selectin Deficiency Attenuates Brain Ischemia in Mice
Author(s) -
Ma XiuJuan,
Cheng JinWei,
Zhang Jing,
Liu AiJun,
Liu Wei,
Guo Wei,
Shen FuMing,
Lu GuoCai
Publication year - 2012
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12000
Subject(s) - medicine , tunel assay , ischemia , apoptosis , myeloperoxidase , western blot , stroke (engine) , endocrinology , inflammation , immunohistochemistry , chemistry , biochemistry , mechanical engineering , engineering , gene
Summary 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 ( SHR s) and stroke‐prone spontaneously hypertensive rats ( SHR ‐ SP s). 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 ‐1β, and TNF ‐α 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 ‐ SP s than in SHR s ( P < 0.05) after salt intake. E‐selectin deficiency improved neurological function and reduced infarct area in cerebral ischemic mice. MPO and IL ‐1β 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.