[Experimental study of evaluation on neuroprotective effect for tetramethylpyrazine against focal cerebral ischemic injury with diffusion-weighted magnetic resonance imaging].

OBJECTIVE: To evaluate the neuroprotective effect of tetramethylpyrazine (TMP) against focal cerebral ischemic injury in rats with diffusion-weighted magnetic resonance imaging (DWMRI). METHODS: Rat models of focal cerebral ischemic injury were established in 16 male SD rats. They were randomly divided into the TMP group and the control group, eight in each group, and pretreated with TMP and normal saline respectively before modeling. Change of infarcted cerebral focus was observed with DWMRI at 1, 2, 6, 12 and 24 hrs after infarction, and the infarction volume (IV) at 24 hrs after modeling was estimated by triphenyltetrazolium chloride (TTC) stain. RESULTS: The IV in all time points observed in the TMP group with DWMRI was significantly smaller than that in the control group (P<0.01). Compared with that at 1 hr after infarction, in the control group at 2, 6, 12 and 24 hrs after modeling, the IV enlarged by 13.3%, 29.7%, 50.3% and 57.3% respectively, while that in the TMP group 9.9%, 21.3%, 37.1% and 40.5% respectively. The cerebral IV estimated by TTC stain 24 hrs after modeling was larger than that estimated by DWMRI. CONCLUSION: TMP pretreatment before modeling was effective in protecting brain against cerebral ischemic damage in rats. DWMRI dynamic scanning observation has important significance in observing the cerebral ischemic developing process and evaluating the effectiveness of brain protective measures.

[Effect of sodium ferulate on activation of extracellular signal regulated kinase after cerebral ischemia/reperfusion injury in rats].

OBJECTIVE: To study the activation of extracellular signal regulated kinase (ERK) after focal cerebral ischemia/reperfusion in rats and the effect of sodium ferulate (SF) on it. METHODS: Forty-five male adult SD rats were randomly divided into 3 groups, the sham-operated group, the control group and the SF group. The model of middle cerebral artery occlusion (MCAO) was established by thread ligation method, and in the ischemic phase, to rats in the sham-operated and the control group 4 ml of normal saline was intraperitoneally injected, and to rats in the SF group, 100 mg/kg of SF dissolved in 4 ml of normal saline was injected. The rats were decapitated at 2 hrs, 6 hrs, 12 hrs, 24 hrs and 72 hrs after reperfusion, 3 rats of every group at each time point, and rats brains were taken for immunohistochemistry and histopathological examination. RESULTS: Histopathological examination showed that the cerebral ischemic damage in the SF group was significantly milder than that in the control group at 2 hrs after reperfusion. The cerebral ischemia induced ERK activation reached the peak at 6 hrs and maintained to 72 hrs after reperfusion. As compared with the control group, the ERK activation in the SF group was significantly enhanced with increased positive immune reacted cells (P < 0.01). CONCLUSION: Cerebral ischemia/reperfusion could induce the activation of ERK in the ischemic brain cells, intervention of SF could enhance the activation and alleviate the ischemic injury in cerebral cortex.