Effect of Panax Notoginseng Saponins on Neuronal Apoptosis and Mitochondrial Apoptosis Pathway Expression c-Jun N-terminal Kinase after Cerebral Ischemia-reperfusion in Mice
TANG Ying-hong, HUANG Xiao-ping, TAN Hua, et al. Effect of Panax Notoginseng Saponins on Neuronal Apoptosis and Mitochondrial Apoptosis Pathway Expression c-Jun N-terminal Kinase after Cerebral Ischemia-reperfusion in Mice[J]. Chinese journal of experimental traditional medical formulae, 2010, 16(16): 129-133.
TANG Ying-hong, HUANG Xiao-ping, TAN Hua, et al. Effect of Panax Notoginseng Saponins on Neuronal Apoptosis and Mitochondrial Apoptosis Pathway Expression c-Jun N-terminal Kinase after Cerebral Ischemia-reperfusion in Mice[J]. Chinese journal of experimental traditional medical formulae, 2010, 16(16): 129-133.DOI:
Objective: To investigate the effect of Panax Notoginseng Saponins(PNS)on neuronal apoptosis and mitochondrial apoptosis pathway and c-Jun N-terminal kinase (JNK) activation after cerebral ischemia-reperfusion injury in mice. Method: C57BL/6 mice were randomly divided into sham-operation group
model group
PNS group and edaravone group.Cerebral ischemia-reperfusion injury was prepared by bilateral common carotid artery ligation for 20 min followed by reperfusion for 24 h and 48 h after drug administration for 4 days.Neuronal apoptosis was determined with Tunel and the expression of p-JNK1/2
cysteine-asparate protease -9(caspase-9)
caspase-3 and cytochrome C (CytC) protein in brain tissue was detected with Western-blot. Result: After cerebral ischemia for 20 min followed reperfusion for 24 and 48 h
the neuronal apoptosis rate was enhanced significantly(P<0.01)
the expression of p-JNK1/2
CytC
caspase-9 and caspase-3 protein in brain tissue was increased (P<0.01).The neuronal apoptosis rate in the PNS group was significantly lower than that of the model group(P<0.01)
the expression of p-JNK1/2
CytC
caspase-9 and caspase-3 protein in PNS group was lower than that of the model group significantly(P<0.01 or P<0.05). Conclusion :PNS could attenuate neuronal apoptosis rate by inhibiting activation of signal transduction of JNK and mitochondrial apoptosis pathway after cerebral ischemia/reperfusion injury in mice.