中文摘要：

目的观察ERK通路阻滞剂PD98059（PD）对心肺复苏（CPR）后大鼠脑组织超氧化物歧化酶（SOD）表达以及脑细胞凋亡的影响。方法采用经食管交流电刺激诱导心室颤动建立大鼠心脏骤停／心肺复苏（CA／CPR）模型，将恢复自主循环（ROSC）的48只大鼠随机分成PD组和模型组各24只，分别静脉注射PD0.3mg／kg及等量生理盐水；选择6只大鼠为假手术组,只行手术操作不诱导CA／CPR。分别于ROSC后12、24、48、72h时各处死6只大鼠，取脑组织；用免疫荧光标记法检测大脑皮层组织SOD1、SOD2荧光密度及Caspase3阳性细胞，TUNEL法检测凋亡细胞。结果与模型组比较，PD组各时点SOD1荧光密度均明显升高（P均〈0．05），PD组ROSC后12、24、48h时SOD2荧光密度均明显升高（P〈均0．05）。ROSC后72h，模型组、PD组Caspase3阳性表达率、脑细胞凋亡率均高于假手术组，而PD组Caspase3阳性表达率、脑细胞凋亡率低于模型组，P均〈0．05。结论PD治疗能提高CA／CPR后模型大鼠脑组织SOD表达水平，抑制脑细胞凋亡。

英文摘要：

Objective To observe the effects of ERK channel blocker PD98059 on the expression of superoxide dis- mutase （SOD） and apoptosis of brain tissues after cardio-pulmonary resuscitation （CPR） in rats. Methods We used the alternating current of the esophagus stimulation to induce the ventricular fibrillation and establish the cardiac arrest/cardiop- ulmonary resuscitation （CA/CPR） model. Forty-eight rats, once spontaneous circulation restoring （ ROSC）, were divided into two groups ： PD98059 （PD） group （ treated with 0.3 mg/kg, intravenous intravenously, n = 24 ） and model group （ in-jected with same amount of normal saline, n = 24）. The control group （SH） was treated without CA/CPR （ n = 6 ）. In each group, we executed 6 rats to obtain the brain tissues at 12, 24, 48 and 72 h after ROSC. The SOD1, SOD2 fluores- cence density and positive cells of Caspase-3 in the cerebral tissues were detected by immunofluorescence labeling method, and the apoptosis by TUNEL labeling method. Results After CPR, the SOD1 fluorescence density of the PD group was all higher than that of model group at each time points （ all P 〈 0.05 ）. The SOD2 fluorescence density of the PD group was significantly increased at 12, 24 and 48 h （ all P 〈 0.05 ）. At 72 h after ROSC, Caspase-3 positive expression rate and the apoptosis rate of the PD group and model group was significantly higher than that of the control group, and the Caspase-3 positive expression rate and apoptosis rate of the PD group was lower than that of the model group （ all P 〈 0.05 ）. Conclu- sion PD98059 can improve the SOD expression and inhibit apoptosis of brain tissues of rats after CA/CPR.