摘要
目的研究蛋白激酶抑制剂H-7对局灶性脑缺血半暗带和核心区半胱氨酸蛋白酶Calpain和Caspase-3活性的影响。方法采用动脉腔内插线法建立大鼠局灶性脑缺血模型,在缺血前15min经脑室给予H-7(125μg/大鼠),测定缺血1h再灌注23h(R23h)时,半暗带和核心区Calpain和Caspase-3的活性、Calpastatin和微管相关蛋白-2(MAP-2)的含量及梗死体积。结果H-7明显降低R23h时半暗带和核心区μ-和m-Calpain及Caspase-3的活性,升高核心区Calpastatin的含量及半暗带和核心区MAP-2的含量,缩小梗死体积。结论H-7通过抑制半暗带和核心区Calpain和Caspase-3的活性,降低局灶性脑缺血损伤。
Objective To investigate the effects of protein kinase inhibitor H-7 on the activation of calpain and caspase-3 in penumbra and core after focal cerebral ischemia in rats.Methods Rats received 1h focal cerebral ischemia by intraluminal filament.H-7 (125μg/rat) was administered intracerebroventricularly 15 min before ischemia.The activities of calpain and caspase-3, the levels of calpastatin and microtubule-associated protein-2 (MAP-2), and the infarct volume were assessed by casein zymography,fluorometry,Western blot analysis,and staining the brain sections with 2,3,5-triphenyltetrazolium chlorides,respectively.Results Compared with ischemic control,H-7 markedly reduced the activities of μ-and m-calpain,and caspase-3, increased the levels of MAP-2 in penumbra and core,and enhanced the levels of calpastatin in core.Moreover,animals treated with H-7 showed a significant reduction in infarct volume.Conclusions These data demonstrate the protection of H-7 against focal cerebral ischemia through inhibiting the activation of calpain and caspase-3.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2009年第2期152-154,共3页
Journal of Apoplexy and Nervous Diseases
基金
北京市自然科学基金资助项目(No.7002013)