Osthole alleviates cerebral ischemia-reperfusion inj ury by suppressing mitochondrial mediating apoptosis
10.7652/jdyxb201701028
- VernacularTitle:蛇床子素通过抑制线粒体介导的凋亡信号途径减轻脑缺血再灌注损伤
- Author:
Jia WANG
;
Jiong ZHANG
- Keywords:
Osthole;
cerebral ischemia-reperfusion injury;
mitochondrion;
ROS;
apoptosis
- From:
Journal of Xi'an Jiaotong University(Medical Sciences)
2017;38(1):131-135
- CountryChina
- Language:Chinese
-
Abstract:
ABSTRACT: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.
