Apoptosis is one of the primary factors in cell death after cerebral ischemia reperfusion, it is an initiative suicide process after the cells receive related signals. There are two major pathways of apoptosis after cerebral ischemia: the intrinsic pathway and the extrinsic pathway, the intrinsic pathway, also called mitochondrial apoptosis pathway, is originated from mitochondrial release of cytochromec and associated stimulation of caspase-3. In the intrinsic pathway, release of CytC leads to the formation of the apoptosome and then promotes the activation of procaspase-9. The clustering of Gentiopicrin procaspase-9 leads to caspase-9 activation. Caspase-9, which is considered as an initiator of the mitochondria-dependent caspase cascade, then activates caspase-3. Caspase-3 can cleave many substrate proteins, such as poly polymerase. Overactivation of PARP after cleavage by caspase-3 leads to DNA injury and subsequently to apoptotic cell death. On the other hand, apoptosis is also regulated 
by a series of protein systems, one of these systems is the Bcl-2 family. Bax, as a major proapoptotic protein in the Bcl-2 family, plays a key role in promoting apoptosis. Bcl-2 protein is an important inhibitor of apoptosis which prevents the release of CytC and Caspase activation. Lycium barbarum polysaccharide, a major active ingredient of Lycium barbarum, has been Epimedoside-A reported to have several pharmacological activities such as anti-oxidative, anti-proliferate and hypoglycemic effect. Our previous study demonstrated that LBP has protective effects on hippocampus neurons model of ischemic cerebral injury in vitro. In the present study, we examined the protective effects of LBP in a model of middle cerebral artery occlusion in mice. Furthermore, we investigated the relations between the effects of LBP and the mitochondrial apoptosis pathway in mice brains after stroke. Nimodipine, as a classic clinic drug in stroke, has shown obviously beneficial effects on active treatment in previous studies. So it was also used as a positive control in this study. Ischemic brain disease has become one of the most devastating diseases which cause high rates of disability and mortality in aged persons. Several harmful pathological changes have taken place in the process of cerebral ischemia, which cause a difficult determination of the more appropriate drug target. Then it is a great challenge to find a novel pharmacological drug with protective effect in cerebral ischemic injury. Traditional Chinese Medicines are proved to have many bioactivities which provide neuroprotective effects in ischemic brain disease. In the present study, we used the method of MCAO-induced cerebral ischemic injury in mice to mimic human cerebral ischemic disease, we further investigated whether LBP had neuroprotective effects in MCAO mice and its pharmacological mechanism related with mitochondrial apoptosis pathway after cerebral ischemic injury. Cerebral ischemia can promote a series of pathological changes in neuronal cells such as mitochondrial membrane depolarization and permeability transition pore opening.