Li Z.,Qingdao University |
Li Q.,Qingdao University |
Guo Y.-L.,Qingdao University |
Qin L.-H.,Beijing University Medical College |
Luan L.-J.,Beijing University Medical College
Acta Anatomica Sinica | Year: 2010
Objective: To investigate the neuroprotective effects of picrodide II 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. Picrodide II (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 picrodide II 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 picrodide II group was smaller than that in the salvianic acid A sodium group (P < 0.05). Conclusion: Picrodide II might reduce cerebral infarction volume and improve the neurological behavioral function through inhibiting the neuronal apoptosis induced by ischemia reperfusion injury.