Fingolimod exerts neuroprotective effects in a mouse model of intracerebral hemorrhage

被引:61
|
作者
Lu, Lei [1 ]
Barfejani, Arnavaz Hajizadeh [1 ,2 ]
Qin, Tao [1 ]
Dong, Qiang [3 ]
Ayata, Cenk [4 ]
Waeber, Christian [1 ]
机构
[1] Massachusetts Gen Hosp, Dept Radiol, Charlestown, MA 02129 USA
[2] Northeastern Univ, Sch Pharm, Bouve Coll Hlth Sci, Boston, MA 02115 USA
[3] Fudan Univ, Huashan Hosp, Dept Neurol, State Key Lab Med Neurobiol, Shanghai 200040, Peoples R China
[4] Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA 02129 USA
关键词
Intracerebral hemorrhage; Stroke; FTY720; Sphingosine; 1-phosphate; Neuroprotection; CEREBRAL-ARTERY OCCLUSION; SPHINGOSINE 1-PHOSPHATE RECEPTOR-1; MULTIPLE-SCLEROSIS; FTY720; FINGOLIMOD; INJURY; APOPTOSIS; EFFICACY; STROKE; CELLS; ACTIVATION;
D O I
10.1016/j.brainres.2014.01.048
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Recent studies have shown that fingolimod (FTY720) is neuroprotective in CNS injury models of cerebral ischemia and spinal cord injury. The purpose of the study was to examine the effect of fingolimod in a mouse model of intracerebral hemorrhage. ICH was produced in adult CD1 mice by injecting collagenase VII-S (0.5 mu L, 0.06 U) into the basal ganglia. Fingolimod (or saline) was given 30 min after surgery and once daily for two days. Three days after intracerebral hemorrhage, brain edema, hematoma volume and the number of apoptotic cells were quantified. In another cohort of mice, brain atrophy was evaluated two weeks following intracerebral hemorrhage. Neurobehavioral tests were performed on the 3rd, the 7th and the 14th day. Fingolimod significantly decreased edema, apoptosis and brain atrophy. More importantly, fingolimod enhanced neurobehavioral recovery. Preliminary experiments showed no difference in the number of inflammatory (CD68-positive) cells between the two groups. In conclusion, fingolimod exerts protective effects in a mouse model of intracerebral hemorrhage; the mechanisms underlying these neuroprotective effects deserve further study. (c) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:89 / 96
页数:8
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