摘要
目的观察蛇床子素(Osthole)对大鼠脑缺血再灌注损伤的作用及机制。方法将50只SD大鼠随机分成假手术组、模型组和蛇床子素(25、50、100mg/kg)组(n=10)。利用物理法评估大鼠脑梗死范围、脑含水量和神经症状,试剂盒检测活性氧自由基(ROS)和ATP酶活性,流式细胞仪检测线粒体膜电位,免疫蛋白印迹法检测Caspase3、Clevage-Caspase3、Caspase9、Clevage-Caspase9、Bcl-2、Bax、细胞质中凋亡诱导因子(AIF)和cytochrome C的表达水平。结果与假手术组相比,模型组脑梗死范围、脑含水量、神经症状以及ROS、Cleaved-Caspase3、Cleaved-Caspase9、Bax、细胞质中AIF和cytochrome C的表达明显增加,而Caspase3、Caspase9和Bcl-2表达以及线粒体膜电位和ATP酶的活性明显降低。与模型组相比,蛇床子素组脑梗死范围、脑含水量、神经症状以及ROS、Cleaved-Caspase3、CleavedCaspase9、Bax、细胞质中AIF和cytochrome C的表达明显减少,而Caspase3、Caspase9和Bcl-2表达以及线粒体膜电位和ATP酶的活性明显增加。结论蛇床子素预处理可减轻脑缺血再灌注损伤,其机制可能与抑制线粒体介导的凋亡信号途径相关。
Objective To observe the influence of Osthole on cerebral ischemia-reperfusion injury and its acting mechanism. Methods We randomly divided 50 SD rats into sham （Sham） group, ischemia-reperfusion injury （IRI） group and Osthole （25, 50, and 100 mg/kg） （Osthole） groups （n = 10）. The neurological symptoms, extent of cerebral infarction and cerebral water content were evaluated by physical approach. The activities of ROS and ATP were examined by the kit; the mitochondrial membrane potential （MMP） was measured by flow cytometry. The expressions of Bax, Bcl-2, Caspase3, clevage-Caspase3, Caspase9, clevage-Caspase9, cytoplasmic AIF and cytochrome C were measured by Western blotting. Results Compared with those in sham group, the extent of cerebral infarction and cerebral water content, changes of neurological symptoms, activities of ROS, and expressions of clevage-Caspase3, clevage-Caspase9, Bax, cytoplasmic AIF and cytochrome C in IRI group were significantly increased （P〈0.05）. However, the activities of ATP, expressions of Caspase3, Caspase9, Bcl-2 and MMP, and ATP activity were decreased （P〈0.05）. Compared with those in IRI group, the extent of cerebral infarction and cerebral water content, changes of neurological symptoms, activities of ROS, and expressions of clevage-Caspase3, clevage-Caspase9, Bax, cytoplasmic AIF and cytochrome C in Osthole group were significantly decreased （P〈0.05）. But the activities of ATP, expressions of Caspase3, Caspase9, Bcl-2 and MMP, and ATP activities were increased （P 〈 0. 05）. Conclusion Osthole pretreatment can attenuate cerebral ischemia- reperfusion injury, which is associated with suppressing mitochondria-mediated apoptosis.
出处
《西安交通大学学报（医学版）》
CAS
CSCD
北大核心
2017年第1期131-135,共5页
Journal of Xi’an Jiaotong University（Medical Sciences）
基金
国家自然科学基金资助项目(No.81401362
81500575)~~
