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探究p38通路在心肺复苏后大鼠脑组织过氧化物岐化酶(superoxide dismutase,SOD)表达过程中的作用以及对脑细胞凋亡的影响。经食道交流电刺激诱导心室颤动(VF)建立大鼠心脏骤停/心肺复苏(cardiac arrest/cardiopulmonary resuscitation,CA/CPR)模型。假手术(SH)组大鼠只行手术操作,不诱导CA/CPR(n=6)。恢复自主循环后的48只大鼠随机分成两组,分别为SKF86002(SKF)组(2.5 mg/kg,iv.,n=24)和模型组(给予等量生理盐水,n=24),每组分别设12 h、24 h、48 h、72 h四个检测时间点,每个时间点6只大鼠。用免疫荧光标记法检测大脑皮层过氧化物岐化酶的荧光密度,TUNEL标记法检测细胞凋亡情况。结果发现:CPR后,SKF组在各时间点的SOD1和SOD2的荧光密度均较模型组较高(p<0.05)。但是CPR后72 h,SKF组的凋亡率明显较模型组高(p<0.05)。表明SKF干预治疗能显著提高心脏骤停/心肺复苏后模型大鼠脑组织的SOD的表达水平,但并不能抑制脑细胞凋亡。
To investigate the role of p38 pathway in the expression of superoxide dismutase (SOD) in rat brain after cardiopulmonary resuscitation and its effect on brain cell apoptosis. Establishment of rat cardiac arrest / cardiopulmonary resuscitation (CA / CPR) model by inducing ventricular fibrillation (VF) via transesophageal electrical stimulation. Sham operation (SH) rats were operated on only without CA / CPR (n = 6). Forty-eight rats were randomly divided into two groups: SKF86002 (2.5 mg / kg, iv., N = 24) and model group (given the same amount of saline, n = 24) Groups were set at 12 h, 24 h, 48 h, 72 h four test time points, each time point 6 rats. Fluorescent densities of peroxisomal dismutase in cerebral cortex were detected by immunofluorescence staining and apoptosis was detected by TUNEL labeling. The results showed that after CPR, the fluorescence intensity of SOD1 and SOD2 in SKF group was higher than that in model group at each time point (p <0.05). However, at 72 h after CPR, the apoptosis rate in SKF group was significantly higher than that in model group (p <0.05). The results showed that SKF treatment significantly increased the expression of SOD in the brain of model rats after cardiac arrest / CPR, but did not inhibit the apoptosis of brain cells.