中国药理学通报2016，Vol.32Issue(4)：548-553,6.DOI:10.3969/j.issn.1001-1978.2016.04.021
CRMP2可通过改善神经细胞凋亡减轻缺血/再灌注大鼠神经功能缺损
CRMP2 alleviates neurological deficit by reducing neuron apoptosis in rats after cerebral ischemia/reperfusion injury
摘要
Abstract
Aim To investigate the influence of the overexpression of CRMP2 on neural cell apoptosis after ischemia reperfusion injury in rats and its possible mechanism. Methods A total of 192 male adult SD rats were divided into four groups: sham group, cere-bral ischemia/reperfusion group( MCAO group) , cere-bral ischemia with blank plasmid control group( MCAO+GFP group ) , cerebral ischemia with CRMP2 eu-karyotic plasmid group ( MCAO + CRMP2/GFP group) . One day after injecting eukaryotic plasmid, the rats were operated for 120-min ischemia through MCA occlusion and reperfused. At 48 h and 1 wk, the expression of CRMP2 , p53 , Caspase-3 , Caspase-8 and BCL2 in brain tissue was tested by RT-PCR and West-ern blot. Apoptotic cells were observed by TUNEL test. TTC staining was use to detect cerebral infarction volume. The neural function of the rats were also eval-uated. Results Compared with the sham group, the expression levels of CRMP2 and BCL2 in MCAO group and MCAO +GFP group were significantly decreased ( P <0. 01 ) , while p53 , Caspase-3 , Caspase-8 and TUNEL positive cells were elevated(P<0. 01). Inter-vention of CRMP2 eukaryotic plasmid resulted in the increased expression of CRMP2 and BCL2 ( P<0. 01 ) and the decreased p53 , Caspase-3 and Caspase-8 ex-pression. In TUNEL test, overexpression of CRMP2 obviously decreased the number of TUNEL positive cells(P<0. 01). The expression of BDNF was upregu-lated after cerebral ischemic injury ( P<0. 01 ) , while overexpression of CRMP2 increased BDNF more signif-icantly ( P <0. 01 ) . TTC staining showed cerebral in-farction volumn of MCAO + CRMP2/GFP group was obviously decreased ( P <0. 01 ) , and neurologic defi-cits were significantly improved ( P <0. 01 ) . Conclu-sion The overexpression of CRMP2 reduces nerve cell apoptosis possibly by regulating the mitochondrial ap-optosis pathway after cerebral ischemia/reperfusion in-jury to protect nervous system.关键词
CRMP2/脑缺血/再灌注/BDNF/凋亡/神经功能评分/TUNELKey words
CRMP2/cerebral ischemia/reperfusion/BDNF/apoptosis/neurological score/TUNEL分类
医药卫生引用本文复制引用
幸享凤,王恬竹,秦新月..CRMP2可通过改善神经细胞凋亡减轻缺血/再灌注大鼠神经功能缺损[J].中国药理学通报,2016,32(4):548-553,6.基金项目
国家自然科学青年基金资助项目(No 81200900) （No 81200900）
