AIM: The aim of this study was to investigate the protective effect of chuanxiongzine-puerarin on cerebral ischemia-reperfusion damage in a rat model. METHODS: Rats were randomized into the following three groups: control group (sham operation group), model group (cerebral ischemia-reperfusion damage group), and treatment group (puerarin group, chuanxiongzine-puerarin group, and nimodipine group). The effect of neurological deficit, infarct volume and levels of superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO), synaptophysin, and interleukin-1 was assessed. The therapeutic effect was also evaluated micro-positive emission tomography with [F]fluoro-2-deoxy-D-glucose. RESULTS: After cerebral ischemia-reperfusion damage, the neurologic deficit score and the infarct volume percentage in treatment group were significantly lower than in the model group (P<0.01). Micro-positive emission tomography imaging showed that glucose metabolism in the right temporal lobe and the right frontal lobe were significantly decreased in the model group in comparison with the sham operation group (P<0.01). After treatment, glucose metabolism increased significantly in the puerarin group and the chuanxiongzine-puerarin group, compared with the model group (P<0.05 and <0.01, respectively). The expression of interleukin-1beta-mRNA was significantly higher in the model group than in the sham operation group (P<0.01). After treatment, however, it was significantly decreased in the puerarin group (P<0.05) and the chuanxiongzine-puerarin group (P<0.01) compared with the model group. SOD activity in the model group (P<0.01) was lower than that in the sham operation group, whereas MDA and NO content in the model group was more than that in the sham operation group (P<0.01). In the chuanxiongzine-puerarin and puerarin treatment groups, SOD activity showed higher level compared with the model group (P<0.01); however, MDA and NO content was decreased in the treatment group (P<0.01). Synaptophysin level was significantly lower in the model group compared with the sham operation group (P<0.01), whereas the chuanxiongzine-puerarin and puerarin groups showed significantly higher values than the model group (P<0.05). CONCLUSION: This study showed that chuanxiongzine-puerarin played an important protective role against cerebral ischemic reperfusion damage in a rat model.
AIM: The aim of this study was to investigate the protective effect of chuanxiongzine-puerarin on cerebral ischemia-reperfusion damage in a rat model. METHODS:Rats were randomized into the following three groups: control group (sham operation group), model group (cerebral ischemia-reperfusion damage group), and treatment group (puerarin group, chuanxiongzine-puerarin group, and nimodipine group). The effect of neurological deficit, infarct volume and levels of superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO), synaptophysin, and interleukin-1 was assessed. The therapeutic effect was also evaluated micro-positive emission tomography with [F]fluoro-2-deoxy-D-glucose. RESULTS: After cerebral ischemia-reperfusion damage, the neurologic deficit score and the infarct volume percentage in treatment group were significantly lower than in the model group (P<0.01). Micro-positive emission tomography imaging showed that glucose metabolism in the right temporal lobe and the right frontal lobe were significantly decreased in the model group in comparison with the sham operation group (P<0.01). After treatment, glucose metabolism increased significantly in the puerarin group and the chuanxiongzine-puerarin group, compared with the model group (P<0.05 and <0.01, respectively). The expression of interleukin-1beta-mRNA was significantly higher in the model group than in the sham operation group (P<0.01). After treatment, however, it was significantly decreased in the puerarin group (P<0.05) and the chuanxiongzine-puerarin group (P<0.01) compared with the model group. SOD activity in the model group (P<0.01) was lower than that in the sham operation group, whereas MDA and NO content in the model group was more than that in the sham operation group (P<0.01). In the chuanxiongzine-puerarin and puerarin treatment groups, SOD activity showed higher level compared with the model group (P<0.01); however, MDA and NO content was decreased in the treatment group (P<0.01). Synaptophysin level was significantly lower in the model group compared with the sham operation group (P<0.01), whereas the chuanxiongzine-puerarin and puerarin groups showed significantly higher values than the model group (P<0.05). CONCLUSION: This study showed that chuanxiongzine-puerarin played an important protective role against cerebral ischemic reperfusion damage in a rat model.