Objective To investigate the neuroprotective effects of picrodideⅡ on cerebral ischemic reperfusion injury in rats. Methods Intraluminal thread methods were applied to establish the left middle cerebral artery occlusion reperfusion models (MCAO/R) in rats. PicrodideⅡ (10mg/kg) and salvianic acid A sodium (10mg/kg) were injected from tail vein for treatment. The neurological behavioral function was evaluated with Bederson's test. The cerebral infarction volume was observed with tetrazolium chloride (TTC) staining. The structure of cells was observed with histopathology. The apoptosis positive cells were counted by terminal deoxynucleotidyl transferase midiated dUTP nick end labeling (TUNEL). Results The neurological behavioral malfunction appeared in all rats with MCAO/R. The infarction focus showed in the ischemic hemisphere following cerebral ischemia reperfusion injury. In the picrodideⅡ and salvianic acid A sodium treatment groups, the number of apoptosis positive cells decreased and the cerebral infarction volume reduced, while the neurological behavioral function was significantly improved than those in the model control group (P<0.05). The cerebral infarction volume in the picrodideⅡ group was smaller than that in the salvianic acid A sodium group (P<0.05).Conclusion PicrodideⅡ might reduce cerebral infarction volume and improve the neurological behavioral function through inhibiting the neuronal apoptosis induced by ischemia reperfusion injury.

Objective To observe the influence of neuregulin-1?(NRG-1?) on neuronal apoptosis and the expressions of signal transducer and activator of transcription(STAT3) and glial fiberillary acidic protein(GFAP) following cerebral ischemia/reperfusion in rats.Methods The animal models of middle cerebral artery occlusion/reperfusion(MCAO/R) was established by the intralumianl filament method from left external-internal carotid artery in adult healthy male Wistar rats.The rat models were treated by injecting 1.5% NRG-1? 5?l from internal carotid artery.The neuronal apoptosis was detected by DendEnd fluorometric TUNEL assay,and the expressions of STAT3 and GFAP were determined by immunohistochemical and immumofluorescent assays.Results The cerebral ischemia/reperfusion injury could induce neuronal apoptosis and the expressions of STAT3 and GFAP in brain tissue.In control group,the number of neuronal apoptosis increased gradually and the STAT3 and GFAP were expressed highly along ischemia times in the cortex,striatum and hippocampus areas.After treatment with NRG-1?,the number of neuronal apoptosis reduced and the expression level of STAT3 and GFAP increased when compared to those in the control group at different ischemia times and corresponding areas(P