Crocin pretreatment markedly improved the neurological dysfunction and decreased the infarct volume in a dosedependent manner in middle cerebral artery occlusion (MCAO) rats. Western blot analysis showed that crocin up-regulated B-cell lymphoma 2 (Bcl-2) expression， down-regulated Bcl-2 associated protein X (Bax) and cleaved caspase-3 expression of hippocampus in MCAO rats. Because oxidative/nitrative stress is a very important factor in ischemiareperfusion (I/R) injury

thus

a sodium nitroprusside (SNP)-impaired PC12 cell model was set up to mimick nitric oxide (NO) excitotocixity in I/R brain. The results showed that crocin protected PC12 cells against SNP-induced cytotoxicity via attenuating the caspase activation and mitochondrial dysfunction  in vitro . Crocin significantly attenuated apoptosis

lactate dehydrogenase (LDH) release

caspase-3 activation

mitochondria membrane potential corruption and the intracellular accumulation of ROS induced by SNP in PC12 cells. Moreover

SNP decreased the expression level of Bcl-2

induced the expression of cytochrome  c  and Bax in PC12 cells

which is similar to the case of hippocampus in MCAO rats; and crocin reversed all these effects. All these evidences support that crocin is an effective agent to protect I/R injury via reasonable mechanism.